Hypertension kc008 hyd

“THE EFFECT OF “KARPASA BEEJADI GRITHA GUTIKA” INTHE MANAGEMENT OF BHRAMA W.S.R. TO HYPERTENSION”

Dissertation submitted in partial fulfillment for the degree of

DOCTOR OF MEDICINE (AYURVEDA)In

“KAYACHIKITSA”

ByDr.B.ARUN KUMAR.

B.A.M.S

GUIDE

Dr. V. VIJAYA BABU.M.D. (Ay.)

Reader,

Postgraduate Department of Kayachikitsa,

Dr. B.R.K.R. Govt.Ayurvedic College,

Hyderabad.

Dr. N.T.R UNIVERSITY OF HEALTH SCIENCES, VIJAYAWADADr.B.R.K.R. GOVT.AYURVEDIC COLLEGE,

HYDERABAD.

2008

created by technoayurveda.wordpress.com of Dr.KSRPrasad

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TAyComprehended

Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCES,VIJAYAWADA.

POST GRADUATE TRAINING AND RESEARCH UNIT

DEPARTMENT OF KAYACHIKITSA

Dr. B.R.K.R. GOVT. AYURVEDIC COLLEGE / HOSPITAL,

HYDERABAD.

CERTIFICATE

This is to certify that the present dissertation embodies the outcome of original

observations made by Dr. B.Arun kumar on “The effect of Karpasa beejadi Gritha

Gutika in the management of ‘Bhrama’ w.s.r. to Hypertension” for the degree of

‘Doctor of Medicine’ (Ayurveda). This work has been completed under my direct

supervision after a series of a scientific discussion.

The scholar has put in commendable effort for designing and executing the methods and

plans for the study. The results achieved through this work are authentic and reproducible. Hence I

recommend this dissertation to be submitted for adjudication.

GUIDE

Date: Dr. V. VIJAYA BABUPlace: Hyderabad. MD (Ayu)

ReaderPost graduate Department of Kayachikitsa,Dr. B.R.K.R. Govt. Ayurvedic College,

Hyderabad.


Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCES,VIJAYAWADA.

POST GRADUATE TRAINING AND RESEARCH UNIT

DEPARTMENT OF KAYACHIKITSA

Dr. B.R.K.R. GOVT. AYURVEDIC COLLEGE / HOSPITAL,

HYDERABAD.

CERTIFICATE

This is to certify that Dr. B.Arun kumar of M.D. (Ayu) Kayachikitsa has worked for the

thesis on the topic ‘The effect of Karpasa beejadi Gritha Gutika in the management of Bhrama

w.s.r. to Hypertension’ as per requirements of the order laid by the N.T.R. University of Health

Sciences, for the purpose. The hypothesis submitted by him in the first year MD (Ayu) is one and

the same to that of the dissertation submitted.

I am fully satisfied with his work and hereby forward the dissertation for the evaluation of

the adjudicators.

Date: Dr.PRAKASH CHANDERPlace: Hyderabad MD (Ayu)

Professor& HOD,Post graduate Dept. of KayachikitsaDr. B.R.K.R. Govt. Ayurvedic College,

Hyderabad.


ACKNOWLEDGEMENT

I take utmost pleasure and feel privileged to express my deep sense of gratitude

and extreme indebtedness to my Guru and Guide Dr. V. VIJAYA BABU, M.D. (Ayu),

Reader, Post Graduate Dept. of Kayachikitsa, Dr. B.R.K.R. Govt. Ayurvedic College,

Hyderabad for his constant and valuable guidance, encouragement throughout the

dissertation work. Undoubtedly the correct, affectionate and untiring guidance of my

Guru has been a greatest asset in its completion.

I express my heartful gratitude to Dr. PRAKASH CHANDER, MD (Ayu), Professor and HOD,PG Dept. of Kayachikitsa, Dr. B.R.K.R. Govt. Ayurvedic College, Hyderabad, for his constant support,guidance, encouragement and kind co-operation in all aspects.

I convey my wholehearted thanks and sincere respect to Dr. V.V.S.Ramashastry,

Dr.M.L.Naidu and Dr.Vasudeva rao, former Guides who guided me in this work.

I take this opportunity to express my sincere thanks to Dr P. Nageswar Babu, Dr. S.

Ramalingheswar Rao Technical Assistants, Post Graduate Department of Kayachikitsa,

for their kind co-operation in my clinical work.

I am highly indebted to Dr.K. VijayaLakshmi, for her valuable suggestions being a co-

guide for my work.

I pay my sincere respect to Dr. M. Sadashiva Rao, principal of Dr. B.R.K.R Govt.

Ayurvedic College, Hyderabad for providing facilities for the research work.

I am thankful to Dr. V.L.N.Shastry, Superintendent, Govt.Ayurvedic Hospital,

Erragadda, Hyderabad, for permitting me to conduct research work in the Hospital.

I am highly thankful to Dr. V. Anantsayanachari, HOD of P.G. Dept. of S.S.P and

Dr. M. Philip Anand Kumar, HOD of P.G. Dept. of Dravyaguna for his kindly co-

operation.


I cordially acknowledge my friends and colleagues Dr. K.Srinivasulu, Dr. Namratha,

Dr. Shirisha, Dr. R.Krishna kumar,Dr.B.Kishan,Dr.A. Yadagir,Dr.Kandagatla and

others who helped me in one way or other in completing this work.

I bow my head on the feet of my mother and father. Due regards My wife Dr.B.Shilpa, my

brothers B.Prasad kumar,B.pradeep kumar and my son Mr. Shashank who always stand

with me in each and every moments of my life. My love and appreciations to my all

nephews and nieces for standing with me all time with love affection and patience.

I am highly grateful to the authors of all the books and articles which were utilized by me

as the source of information in the preparation of this thesis.

Lastly I am thankful to all my patients for volunteering trial and all those persons, who

have helped me directly or indirectly for this project work.

Dr.B. Arun kumar.Date:

Place: Hyderabad


LIST OF TABLES:

S.No. Title of the table Page No.1. Table showing the external features of the heart 112. Diagram showing difference between artery and vein. 163. Illustration showing the blood pressure regulation. 204. Illustration showing the ‘rennin-angiotensin system’. 235. Showing the phases of ‘korotkoff sounds’ 286. Schematic representation of ‘samprapthi of bhrama’ with special

references to hypertension.56

7. Table showing the hypothetical scheme for the pathogenesis ofessential hypertension.

65

8. Table showing initiation of modern treatment in patients withhypertension.

78

9. Table showing classification and management for Adults 809. Table showing picture of individual drugs 92

10. Incidence of sex 10111. Incidence of age 10212. Incidence of religion 10313. Incidence of marital status 10414. Incidence of occupation 10515. Incidence of socioeconomic status 10616. Incidence of food habits 10717. Incidence of addictions 10818. Incidence of family history 11019. Incidence of availability 11120. Incidence of habitate 11221. Incidence of severity before treatment 11322. Incidence of obesity 11423. Incidence of chronicity 11524. Incidence of prakriti 11625. Incidence of stress 11726. Incidence of diabetes mellitus association 11827. Incidence of using other drug 12028. Table showing the subjective parameter bhrama 12229. Table showing the subjective parameter Shirahshula 12330. Table showing the subjective parameter Anidra 12331. Table showing the subjective parameter Over all symptoms 12332. Table showing results based on subjective parameter 12433. Table showing results based on systolic blood pressure 12534. Table showing results based on diastolic blood pressure 12635. Table showing results based on objective parameter. 127


INDEX

Page no.

Introduction 1.

Historical Aspect 3.

PART-A: Shaariram

1) Anatomy of Heart and Blood vessels. 08

2) Physiology of blood circulation. 17

3) Regulation of blood pressure. 20

4) Measurement of blood pressure. 25

PART-B: Disease Aspect

1) Nirukthi & Paribhasha of “Bhrama” 29

2) Nidana. 33

3) Purvarupa. 46

4) Rupa. 47

5) Samprapthi. 50

6) Sapeksha nidana. 69

7) Upadrava. 71

8) Diagnosis and Assessment. 73

9) Chikitsa. 75

10)Pathya-Apathyas 82


PART-C: Drug Profile

1) Criteria for the selection of the drugs 83

2) Description of the individual drugs 84

3) Mode of preparation of compound drug and

administration. 94

PART-D: Clinical study.

1) Materials and Methods 95

2) Observations and Results 99

3) Discussion 128

4) Conclusion 136

5) Summary 138

Bibliography. 139

Annexure. 146


1

INTRODUCTION

The word “Hypertension” is a hybrid of the greek and Latin origin means” Over

stretching of the arteries”. This malady is mostly observed in civilized societies or literate

persons. Who generally force increased socioeconomic stress and strain, irregular dietary

habits and competitive profit motivated, industrialized way of life, so that it is called as a

disease of high pressure society. If it is untreated hypertension takes twenty years off the

average life expected. Where males are far worse than females. Hypertension doesn’t

matter for itself but its outcome, so that it is nicknamed as “silent killer” in aim of the

consequences, along with the increasing of upper age groups of population. However

hypertension became the most common cardiovascular disorder.

It is an established fact that heart and blood vessels are directly involved in

hypertension but it may be essential or secondary, whatever may be role of various

hormones, baroreceptors, chemoreceptors, sodium, blood volume, and viscosity, renin

angiotensive system, vascular disease(Atherosclerosis),vascular reactivity.

Regarding the hypertension one can’t find out the word corresponding to it in

ayurveda. Charaka mentioned that vata, pitta, kapha only cause the nija vyadhis. He

mentioned “Bhrama” in Vataja nanatmaja vyadhis. Sushrutha stated that without dosha,

there will be no disease, by this dosha predominance, in their capacity to produce the

disease can be observed in accordance to their lakshanas for the causation of any disease,

pertaining to the thri vidha roga margas, vata holds responsibility, without vata, there will

be no disease. Even pitta and kaphaja vyadhis that too, the lakshanas enlisted for the

disease hypertension are showing the vata and pitta predominance like

“bhrama”,rakvavritha vata,Pittavrita vata etc.,

The ultimate results are 2, i) increased cardiac output and ii) increased peripheral

resistance, unless these two symptoms are there in hypertension that cannot be considered

according to modern and ayurveda.


2

However a critical and careful study of the ayurvedic classics confirms that

hypertension is merely a collective concept for a number of conditions having in common

the positive characters of arterial hypertension like Raktavrita vata or Raktagata vata,

siravata, Pittavrita vata,Kaphavrita vyana vata.

Hypertension which pertains to sakhas (tissues) is a bahyaroga marga disease.But

it may involve the madhyama roga marga also comprising the three vital organs or

marmas like basti, siras and hridaya.

All most all surveys show that blood pressure rises with age in both men and

women. A national study showed that 76% of the male hypertensive and 88%of females

were in the age group of 25-60yrs.Framingham study showed that an average of 20-

mmofHg systolic and 10mmofHg diastolic increase from age 30-65yr.

Hypertension is one of the most important modifiable risk factors for coronary

heart disease in western and Asian population. Studies from India have shown an

increasing trend in the prevalence of hypertension. Community surveys have documented

that in a period of three to sex decades, prevalence of hypertension has increased about

30 times among urban dwellers and by about 10 times among the rural inhabitants. The

various studies estimated a prevalence rate of hypertension among urban population

ranging from 1.24%in 1949to 36.4%in 2003, and for rural people from 1.99%in 1958 to

21.21%in 1994. The sentinel surveillance project documented 28% overall prevalence of

hypertension (Criteria=JNCVI) from 10 regions of the country in the age group 20-69.

The present study is “The Effect of Karpasabeejadi Gritha Gutika” in the

management of “bhrama” w.s.r. to Hypertension”. To assess the efficacy of the drug in

the maintenance and management of bhrama i.e., Hypertension and the effect of relief

giving in subjective symptoms i.e., relief in bhrama, headache and sleeplessness etc,


3

HISTORICAL ASPECT:

If you just look back to the past days the clinical entity of hypertension is not

available as such in any of the classical literatures of ayurveda. We find more than

thousands of diseases described in ayurveda which can be correlated or resembles one or

the other modern diseases like jwara, rajayakshma, vvisarpa, switra etc., to that of fever,

tuberculosis, herpes, leucodermas etc., respectively. On the contrary it is difficult to find

a clearcut correlation to that of hypertension in our science. But looking to the description

of hridaya, the disease like hridroga, pakshagatha which can be taken as the

complications of hypertension and the drugs like sarpagandha, arjuna etc., we can think

of hypertension to be present in those days.

PREVEDIC PERIOD:

In prevedic period we don’t find any reference regarding hridroga, hrudaya or any

cross references regarding hypertension.

VEDIC PERIOD:

In vedic period we do find references in “atharvaveda” regarding hrudaya,sira,

dhamani,rasa samvahana and the diseases like hridaya, pakshagatha etc., and we can see

some special treatments adopted for these. From this point of view we can think of

hypertension to be present in those days.

PURANA AND UPANISHA PERIOD:

In purana and Upanishads also we cone across the descriptions regarding the

hridaya its disorders etc., in agni purana, skandapurana, mandookopanishad, katopanisha

etc.,

SAMHITA PERIOD:

The description of“Bhrama” in so many disorders is discussed in Charaka samhita

and Sushritha samhita. In “Charaka” the most references are seen in Chikitsa stana,

Vimana and nidana stana. During the treatment of bhrama in so many places grithas are


4

described by charaka. eg., Rohinyadi gritha, Triphaladi gritham and Duralabhadi gritha.

In vatarakta and trishna chapters’ bhrama mentioned as a upadrava. Most of the

descriptions of bhrama are seen in jwara chapter by charaka.

In “sushritha samhita” the most of the descriptions are seen in sutrastana only.The

scientific era of ayurvedic medicine is the samhita kala in this kala the most scientific

approach and thoughts evolved regarding disease, treatment and basic principles etc.,

Some of the samhitas like charaka samhita, sushrita samhita, kashyapa samnita,

bhela samhita were popular during that period. In all these we get references regarding

hridaya, siradhamani, rasa samvahanaie, circulating mechanism and its disorders. Along

with these some of the disorders which are correlated by present day authors, based on

the modern clinical features of hypertension like raktavrita vata, raktagata vata, avrita

vata, dhamani pratichaya etc., are also available in these samhitas.

Even acharya charaka while mentioning the upadravas of avrita vata in chikitsa

stana 28th chapter he mentions “hridroga” as one among them. This suggests that achrya

had the idea regarding hypertension.

According to one of the well known modern physiology author dr.choudhary in

his book “concise medical physiology” describes hypertension is an ancient disease more

than 2500 yrs ago, charaka the father of Hindu system of medicine, described the

condition admirably. But here the author is not clear regarding the context or reference in

charaka samhita.

Supporting the above view it is found that based on the dissection of ancient

Egyptian mummies high blood pressure has been a health problem since at early

Egyptian empires. And in the yellow emperor classics, 2600 BC ago. It is found “the

blood current flow continuously and never stops and if too much salt is used the pulse

hardens.


5

Regarding understanding and concept of this disease rather than to say they did

not had the knowledge or concept we can say that they did not thought much regarding

this since it was not the major problem or disease during those days. Because of the

following reasons.

i)The people during these days used to line in agrarian civilization where they had

enough time to follow daily routines like dhinacharya, rutucharya, sadvritta etc.,

ii)As such there was no industrial civilization and there fore mental stress was not

seen as much as in the present days. This may be one of the reasons for the disease not

being found.

For want of above reasons the disease probably did not manifest so rapidly so as

to attract the attention of the medical people. Therefore no specific description about a

disease resembling hypertension is found in classical literatures.

Apart from this the instruments like sphygmomanometer, electric device or

automated ambulatory blood pressure devices were not there during those days which is

of prime importance in detection of hypertension in asymptomatic.

However it does not mean that a disease not described in our science cannot be

seen at any time in future. Probably our “acharyas” had the intuition that kind of diseases

may manifest or develop in future due to various changes in environmental, cultural or

socioeconomic factors etc.,

Acharya charaka and sushritha have explained beautifully regarding approach of

such diseases i.e., the physician should not get disheartened if he does not know the name

of a disease, instead he should try to collect the information with regards to signs and

symptoms, causes and relate them to tridoshas ie., they mean to say that the concept of

that particular disease should be understood.

After deciding the relation between doshas and an unknown disease, on the basis

of above lakshanas or features the physician should chart out the management of doshas.

This as a guiding principle can help us theoretically to evolve the etiopathogenisis and its

management.


6

SANGRAHA PERIOD:

In this period the one of the most popular book is “Astanga hridaya”. In this book

the description of “bhrama” is seen in so many places i.e.,jwara, visarpa, raktapitta,

Pittaja kasa,Pitta and sannipataja udara,Vataja murcha and Vataja trishna.

This period has been regarded as an “era of inflorescence” of Indian medicine.

Astanga sangraha and astanga hridaya are the granthas of this period. Even in these two

also we do get references regarding the avrita vata and other correlated diseases at

different contexts.

COMPILATION PERIOD:

“Madhava nidana” describes bhrama in various chapters with different context.

He mentioned bhrama as asadya lakshana in madatyaya. It is mentioned as upadrava for

ajirna, vatarakta, amavata and hridroga. In “Sharangadhara samhita” bhrama mentioned

as one of the bheda of murcha.

In this period we find books like madhava nidana, sharangadhara, yogaratnakara

etc., even in these books we do get references regarding the avrita vata and other

correlated diseases which are dealt at later stage.

ADHUNIKA KALA:

The history of hypertension dates back to 16th century when disease of the heart

and blood vessels were recognized after post mortem examination. When church began to

permit autopsies. But it was in the 2nd century AD. Gallen described almost all the

abnormalities of pulse recognized today which can be thought of here. The arterial blood

pressure gained importance in medical science after “Stephen hales” first measured it in

1733. The blood pressure cuff was invented in 1896. A little more than 100 yr “Riva

rocci” invented the clinical sphygmomanometer and almost 100yr since “korotkoff”

described the auscultatory sounds, major changes in this most commonly performed

procedure in clinical medicine are underway.


7

It was not until the 1950’s that we become aware of the importance of high blood

pressure as a herald of the complications commonly attributed to old age. Regarding the

treatment modern era of antihypertensive therapy began only a little over 50yr ago. With

the pioneering work of “Freis” in the unitedstates and “Smirk” in Newzeland regarding

the level of blood pressure. Sir george pickering in 1972restated that there is no dividing

line between normal and high blood pressure the higher the pressure worse the prognosis.

Presently hypertension is the major risk factor in the development atherosclerotic

IHD and cerebrovascular disease. The researches on this are still going on with to days

update as tomorrows outdate.

In this adhunika kala our 20th century authors have correlated this disease based

on symptomatology with various diseases and conditions told in our science. Though

they could not seemed it correlating exactly to that of essential hypertension, with few

signs and symptoms they have tried to correlate it. Some authors have just translated the

term essential hypertension to some terminologies.


8

SHAREERAM:

ANATOMY OF HEART:

The word hridaya explains and signifies only the functional aspect of an organ.

According to “shatapada brahmana the word hridaya is made up of three dhatus Hri,Da

and Ya. These dhatus by the combination of the pratyaya and adesha, forms the dhatus as

Hrit, Dana and Ayana.

The dhatu Hrit gives the meaning of Harana, Apatirite i.e.,to take or to receive.

The dhatu ‘Dana’ gives the meaning of Tyage, palane, chedane i.e., to give or to eject or

to nourish. The dhatu ayana having the paribhasha of kayam gives the meaning of Gati,

chalana or movement.

The word “hridaya” has been attributed to mainly two organs.Namely Mashtishka

or shirohridaya and hridaya i.e., Uro hridaya. Generally yogis attribute the word hridaya

to Mashtishka or brain and the physicians or Vaidyas denote the word hridaya to

urohridaya or Muscular heart.

In classics the anatomy and physiology of hridaya is not explained under one

heading or at one place. We get lot of quotations and similies based on which we should

understand the anatomy and physiology of heart.

Hridaya is considered as one of the koshtanga. It is situated in vaksha pradesha in

between the two stanas1. It formed by sleshma and rakta2 having the shape of inverted

lotus3 and according to arunadatta it is made up of mamsapeshi and rakta.4 It measures

two angula according to chakrapani and four angula according to sushritha.

Hridaya is the mula of pranavaha and rasavaha srotas5. It is the seat of manas and

para and apara ojus6. Hridaya is the prabhava sthana of dashadamanis which spreads all

over the body and which carries rasa, ojus and does tarpana karma7. According to

palakapya from hridaya siras arise and spreads all over the body justlike a network and

like all rivers join ocean in the same fashion all siras opens into hridaya8. Hridaya

continuous to work whether the person is in jagrutavasta or swapatavasta9.


9

Relation of Hridaya with Doshas:

Hridaya is related with all the three doshas. Among vata, it is related with

udanavayu, prana vayu and vyana vayu. Among pitta, it is related with sadhaka pitta and

pachaka pitta and among kapha it is related with avalambhaka kapha.

Hridaya and udana vayu

Charaka and Vagbhata have mentioned the uras as the sthana of udana vayu10.

This indicated that it is related to hridaya also. When we look at the functions of udana

vayu, the functions like prayatna(endeavour or effort),urja(enthusiasm)and

bala(strength)11, with respect to hridaya, we can think of the conductive system of the

heart i.e., udana vayu by the functions like prayatna and bala initiates and helps in the

conduction of the cardiac impulses in the heart.

Hridaya and prana vayu

According to Charaka and Vagbhara prana vayu is situated in shiras12, and

according to Sharangadhara it is situated in hridaya13.Vagbhata states that pranavata

maintains the activities of hridaya (heart and circulatory system) and supports or does

dharana of dhamanis(probably the vasomotor functions)14.Looking to the above

description it can be said that pranavata situated in murdha sends impulses to hridaya,

there by governing the sympathetic and parasympathetic actions/functions.

Hridaya and Vyana vayu

Vyana vata is situated in hridaya15, and it pervades swiftly throughout the body16.

Vyana vayu is responsible for circulation of Rasa (rasadhatu) through out the body17,by

the regular contraction and relaxation of the heart18. Sushrutha has also mentioned asruk

sravana to be one of the functions of vyana vayu19.Vagvhata concised all functions of

vyana vata by the statement that all the actions or movements of the body are conducted

by vyana vata20.

In Naadi gnynam it is mentioned that the rhythmic tendency of the heart is

responsible for continuous contraction and dilation of the hridaya and which is the

inherent tendency and capacity of hridaya. Enen Charaka has mentioned that vyana vayu


10

is responsible for the continuous flow of rasadhatu to all parts of the body through out the

life by using the words like ajasram and sada21.

Hridaya, Sadhaka pitta and Manas

Sadhaka pitta is situated in hridaya22, and it is responsible for achievement of

buddhi, medha, abhimana, utsaha and abhipretartah. From this it is understood that, it is

essentially connected with some of the higher mental faculties and emotional states. The

concept of sadhaka pitta therefore, encompasses psycho-physiological actions. It is also

seen that hridaya is the adhisthana of manas23. Acharya Charaka while mentioning

measures to protect hridaya and oja says to void the things that produces dukh to the

manas24.Even in unmanda chikitsa adhyaya also acharya charaka mentions about

manovaha srotas. Chakrapani commenting on it says the dhamani’s that orginate from

hridaya or the dhamani’ that are related to hridaya desha, are to be taken as manovaha

srotas25. From all these it is clear that hridaya, sadhaka pitta and manas are related to each

other and the vitiation of one causes the vitiation of other.

Hridaya and Avalambaka Kapha

Avalambaka kapha is situated in uras26.It does avalambana of hridaya i.e., with

the help of rasa it gives bala to hridaya. In other way it does tarpana and kledana of

hridaya and there by helping it to function properly.

Relation of Hridaya with Ojas

In shareera ojas has been classified in to two types, i.e., para ojus and apara ojus.

Para ojus is situated in hridaya27. It is asta bindu in pramana and it is said to be uttama

pranayatana (most important vital part). Even, if little of it is destroyed the body cannot

exist. Aprara ojus is situated in hridaya and dhamani and circulates all over the body. It is

ardhanjali in pramana and the deficiency of this ojus does not cause death but diseases

like prameha are likely to set in.

Looking to all these above references we cannot get a clear cut picture of anatomy

and physiology of heart. But it gives a clear idea that, the hridaya that is described is


11

nothing but the muscular heart or cardia. Even the classical quotations given for hridaya

almost fulfil the modern description that has been given for heart.

Heart is a conical, hollow muscular organ, situated in middle mediastinum. It is

enclosed within the pericardium. The heart is placed obliquely behind the body of the

sternum and adjoining parts of the costal cartilages. So that 1/3rd of it lies to the right.

2/3rdto the left of the median plane. The direction of blood flow, from atria to the

ventricles is downwards, forwards and to the left. The heart measures about 12X9 cm

(5X3 or 3 ½ inches) and weighs about 300gm in males, 250gm in females.

External features:

The human heart has four chambers. These are right and left atria and the right

and left ventricles. The atria lie above and behind the ventricles. On the surface of the

heart they are separated from the ventricles by an atrioventricular groove.

The atria are separated from each other by an interatrial groove. The ventricles are

separated from each other by an interventricular groove. This is subdivided into anterior

and posterior parts. The upper part of each atrium has an appendage called the auricle.

The heart has an apex directed downwards, forwards and to the left; a base (or posterior


12

surface) directed backwards, and anterior, inferior and left surfaces. The surfaces are

demarcated by upper, lower, right and left borders.

The heart is supplied by two coronary arteries, arising from the ascending aorta,

both arteries run in the coronary sulcus. The venous blood is drained by great cardiac

vein, the middle cardiac vein, and the small cardiac veins. The posterior vein of the left

ventricle, the oblique vein of the left atrium, the right marginal vein, the anterior cardiac

veins and the venae cordis minimae. All these except last two drain into the coronary

sinus which opens into the right atrium. The anterior cardiac veins and venae cordis

minimae open directly into the right atrium.

Parasympathetic nerves reach via the vagus. These are cardioinhibitory; on

stimulation they slow down the heart rate. Sympathetic nerves are derived from the upper

3.5 thorasic segments of the spinal cord. These are cardio acceleratory and on stimulation

they increase the heart rate, and also dilate the coronary arteries. Both parasympathetic

and symnpathetic nerves from the superficial and deep cardiac plexus, the branches of

which run along the coronary arteries to reach the myocardium.

REFERENCES:

1. Sus.sam.Sha-6/25

2. Susrita sam.Shari-4/31

3. Sus.sam.Sha-4/32

4. Asta.hri.Sutra-12/15. Arunadatta comment.

5. Cha.sam.Vima-5/

6. Cha.sam.Sutra-30/7

7. Asta.hri.Shar-3/15; Cha.sam.Sutra-30/

8. Paalakapya-16/41.

9. Sus.sam.Shari-4/32.

10. Cha.sam.Chi-28/7; Asta.sam.Sutra-20/4; Asta.Hri.Sutra-12/5

11. Cha.sam.Chi-28/7


13

12. Cha.sam.Chi-28/6; Asta.Hri.Su-12/4

13. Sharanga.Purva khanda-5/27,28 Adhamalla tika

14. Asta.Hri.Su-12/4,5;Asta.San.sutra-20/4

15. Asta.San.Su-20/4;Asta.Hri.Su-2/6

16. Cha.sam.Chi-28/9; Susritha sam.Nidana-1/17

17. Cha.sam.Chi-28/9; Susritha sam.Nid-1/17-18

18. Susritha sam.Sutra-15/3

19. Susritha sam.Nidana-1

20. Asta.Hri.Sutra-12/7

21. Cha sam.Chi-15/36

22. Asta.sam.Sutra-20/5;Asta.Hri.Sutra-12/11;Susritha sam. Sutra-21

23. Cha.sam. Sutra-30/4;Susritha sam.Sharira-4/31;Asta.sam.Su-12/15


25. Cha.sam.Chi-9/5.Cha.sam.Indriya-5/41

26. Astanga hridaya Sutra-12/15-16;Sushrita samhita Sutra-21/13

27. Cha.Sam,Sutra-30/7


14

ANATOMY OF BLOOD VESSELS:The concept of blood vessels in our science has not been cleared till today. It has

been discussed under different headings by different acharyas.

While dealing about the blood vessels or raktavahinis the three terms that are used

are siras, dhamanis and srotas. These three are used with different meanings depending

on the context at different places.

Dalhana in Dhamanivyakharana adhyaya has described regarding sira, dhamani

and srotas elaborately. He has differentiated these then based on four pramanas,i.e.,

lakshana,mula,karma and agama. Dalhana ginving the reason for these three being read

together says though they are differentials yet have similarity in vahanakarma.

Different acharyas have given their opinion regarding these sira, dhamani and

srotas.

A Bird view on views and considerations of different acharyas on sira,dhamani

and srotas.

SIRA DHAMANI SROTAS

Definition:

“Saranaat sirah1”

Chakrapani,gangadh

ara,gananathsen’s

Opinion gives in favour of

vein.

Asudda raktavahinis

are considered as

sira and canbe

referred as

vein(atharvaveda)

Pittavaha siras canbe

considered as vein4

The word sira has

“Dhmand dhamanyah2”

Chakrapani,gangadh

ara,gananathsen’s


artery.

Shudda raktavahinis

are considered as

dhamani and canbe

referred as

artery(atharvaveda)

The word dhamani

has been used with

the meaning of

“Sravanath srotamsi3”

Chakrapani,gangadh

ara,gananathsen’s


capillaries.

It has paryayas like

sira,dhamani,rasaya

na,nadi,pantha,marg

a etc.,


15

been used with the

meaning of

kandara5.

The word sira has

been used with the

meaning of

dhamani6.

The word sira

denotes vein, artery

and lymphatics7.

jnyanatantuvu8.

At parishad

shabdartha it was

concluded that

dhamani canbe

considered as artery,

nerve or vein or any

vessel in the body.

The word dhamani

has been used with

the meaning of

rasavahini9.

The word dhamani

has been used with

the meaning of

sira10.

When we conseder all these references and considerations it is very difficult ot

come to a conclusion,whether sira could be considered as artery or dhamani could be

considered.

Acharya charaka is more of the opinion of considering dhamani to be as artery,

while sushritha considers rohini sira or asrigvaha sira as the artery. Even the parishad that

was conducted on shabdartha could not conclude on this controversy.

The whole circulatory system from the finest capillaries upto and including the

heart is lived by a smooth, continuous single layered endothelium. The walls of all

vessels except capillaries and sinusoids are formed by three analogous zones (coates)

from inside outwards the tinuca intima, tunica media and tunica adventitia. These coats

confer on the vessels a number of important properties, including an endothelial lining

low in friction and connective tissue components able to withstand longitudinal and

circumferential stresses due to prevailing blood pressures.


16

DIFFERENCE BETWEEN ARTERY &VEIN

The smallest arteries terminate in muscular arterioles 100-50um in

diameter,which branch into terminal arterioles less than 50um in diameter. Metaarterioles

are branches of terminal arterioles,10-15um,where they open into the capillary bed. They

are surrounded by a strong circular layer of non striated myocytes forming precapillary

sphicters,which effect the final control of blood flow through the capillaries. Precapillary

sphincters have been seen to open and close periodically with a cycle of 2-8 seconds.


17

REFERENCES:

1. cha.sam.Sutra-30/12. chakrapani comment.

2. cha.sam.Sutra-30/12. chakrapani comment

3. cha.sam.Sutra-30/12. chakrapani comment

4. Susrita sam.Sha-7/18

5. Sus.sam.Nidana-1/82

6. Sus.sam.Sha-7/14

7. Cha.sam.Chi-12/8

8. Sus.sam.Nidana-1/51,85

9. Sus.sam.Sha-9/12

10. Sus.sam.Sha-4/65.

PHYSIOLOGY OF BLOOD CIRCULATION:Hridaya is the srotolula of rasavaha and pranavaha srotas1. It is responsible for

rasa samvahana in the body.

The ahara rasa that is formed is brought to hridaya by samana vayu and this as it

enters the hridaya at is considered as rasadathu. Now with the help of vyana vayu and

udana vayu the sankocha and vikasa i.e., the praspandana of hridaya starts. This function

of it can be correlated to the conductive system of the heart. Here sankocha can be

considered as systole and vikasa can be considered as diastole. Pranavata maintains the

actions of hridaya and does dharana of dhamanies. This indicates that it governs the

vasomotor functions. Once the sankocha takes place the rasa moves into dasha dhamani2

and proceeds further. Here by prasarana akunchana karma and as per kedarakulya nyaya.

The rasa moves to all parts of the body and nourishes the whole body. This function is

carried out continuously throughout the life3.Even Bhela explains that rasa samvahana

takes place through siradhamani, which are spread all over the body and owes their origin

and insertion to hridaya. Sharangadhara while explaining rasa samvahana explains that

rasa, rakta, oja, sneha are carried from hridaya to all parts of the body and does tarpana

karma. Avalambaka kapha gives bala to hridaya to carryout these functions.


18

Regarding rasa samvahana acarya sushritha gives a simily i.e.,”Shabdharchi

jalasantanavat4”.This indicated that rasa moves in all directions. Dalhana commenting on

it says, Urdhwagamitwa of rasa occurs like archi, Adhogamitwa of rasa like jala and

Tiryakgamitwa of rasa lika shabdha.

Again this rasa is brought back to the hridaya by vyana vayu.Samana vayu and

hridaya vikasana takes place followed by sankocha and rasa moving towards sarva

sharira. This cycle continuous and acharya charaka uses the word ajasra to denote

continuous function of hridaya in circulation of rasa5.

The activity of the organs of the circulatory system that is of the heart and blood

vessels ensures a constant flow of blood in the organism. Because of its movement, the

blood can perform numerous transport functions, in particular, supplying oxygen and

nutrients to the tissues and removing substances formed as the result of metabolism.

The movement of blood in the organism follows a complicated course known as

the systemic or greater circulation and the pulmonary or lesser. The systemic circulation

starts at the left ventricle of the heart, passes to the aorta, to the arteries, originating from

it and to all their branches, there to the arterioles, capillaries and the veins of the whole

body and finally to the two venaecavae which enter the right atrium. The pulmonary

circulation begins from the right ventricle, continuous along the pulmonary artery and all

its branches, then along the pulmonary arterioles, capillaries and veins and terminates in

the pulmonary veins which empty into the left atrium.

The flow of blood in the vessels is due to the work of the heart. Contraction of the

ventricular myocardium ejects blood under pressure from the heart into the aorta and

pulmonary arteries. The movement of the blood further along the vessels and its return to

the heart is conditioned by its pressure in the large arteries being higher than in the small

arteries. The pressure in the latter is being higher than in veins and atria. In this way there

is difference in pressure all along the blood stream. That determines its circulation in the

vascular system. Blood flowing from the vessels of higher pressure to those with the

lower pressure. The gradual drop in the pressure along the blood stream (from the arteries

to the capillaries and veins) is brought about by the fact that the energy imported by the

heart is utilized to overcome the resistance of the vessels to the movement of the fluid


19

arising from friction between the fluid particles and the vascular wall and between the

particles themselves.

The function of the heart is rhythmic pumping of blood that it receives from the

veins into the arteries. It is performed by alternate rhythmic contraction and relaxation of

the muscular fibres that forms the walls of the atria and ventricles contraction of the

myocardium of these chambers is known as their systole and relaxation as their diastole.

In normal physiological conditions systole and diastole occurs in a definite

coordination and constitute the cardiac cycle. Each cycle is considered to start with the

atrial systole. The contraction begins as a wave in that part of the right atrium where the

orifices of the venecavae are and then involves both atria which have a common

musculature with a cardiac rhythm of 75 contractions per minute; an atrial (auricular)

systole lasts 0.1 second. As it ends, the ventricular systole begins the atria then being in a

state of diastole which lasts 0.7 second. The contraction of the two ventricles occurs

simultaneously, and their systole persists for about 0.3second. After that ventricular

diastole begins and lasts about 0.5 second. One tenth second before the end of the

ventricular diastole a new atrial systole occurs, and a new cycle of cardiac activity begins.

REFERENCES:

1. Cha.sam.Vimana-5

2. Cha.sam.Chi-15/30

3. Cha.sa.Chi.15/36

4. Sus.sam,Nidana-14/

5. Cha.sam.Chi-15/36.


20

REGULATION OF BLOOD PRESSURE:Physiologically the magnitude of the arterial pressure depends on two

fundamental hemodynamic variables; cardiac output and total peripheral resistance. In

other words, the arterial blood pressure is a product of cardiac out put and peripheral

vascular resistance.

Illustration showing the blood pressure regulation:

Humoral factorsBlood volume Constrictors Dilators.-Sodium -Angiotensin II

-Prostaglandins-Mineralo corticoids -Catacholamines -Kinins-Atriopeptine -Thromboxane -NO/EDRF*

-Leukotriens-Endothelin

BP=Cardiac Out put X Peripheral Resistance

Neural factors Local factorsCardiac factors Constrictors Dilators -Autoregulation.-Heart rate -αadrenergic -βadrebergic -Ion(HP,Hypoxia)-Contractility

*Endothelin derived relaxing factor.


21

The blood pressure can be raised by increased peripheral resistance and by

increased cardiac output.

The cardiac output depends upon the heart rate, its contractibility and the blood

volume. The blood pressure can be raised by an increase in the volume of fluid

absorption of water and water retaining sodium from the intestine in to the vascular

system or and increased production of the adrenocortical hormonal aldosterone, which

blocks the excretion of sodium and water into the urine.

It appears that most patients with established hypertension have abnormal cardiac

output and blood pressure is mainly sustained by increased peripheral vascular resistance.

The peripheral vascular resistance is determined by the arteriolar lumen, which

may expand or contract depending on the state of muscular cells in the vessel wall. This

is known as local vascular tone. Normal vascular tone depends on the competition

between vasoconstricting influences and vasodilators. Peripheral resistance depends on

the size of the lumen of some vessels. A decrease in the inner (lumen) diameter will raise

the blood pressure. The decrease in the lumen could be brought about by an anatomical

thickening of vessel walls (eg, intima thickening of arteries), by their mechanical

compression from outside or most commonly by their active muscular contraction which

cab be induced by a variety of vasoconstrictor mediators. The common vasoconstricting

mediators are epinephrine, norepinephrine and rennin-activated angiotensin II. The other

recently described vasoconstrictors include endothelinI, thromboxane and leucotrienes.

Resistance vessels also exhibit auto regulation, a process by which increased blood flow

to such vessels induces vasoconstriction, an adaptive mechanism that protects against

hyperperfusion of tissues. The vasodilators include kinins, prostagandins and nitric oxide.

Certain metabolic products such as lactic acid, hydrogen ions, adenosine and hypoxia can

also function as local vasodilators.

Recently it has been discovered that haemoglobin plays an important role in

regulation of blood pressure. In the body tissues, haemoglobin releases oxygen and super

nitric oxide (SNO) and picks up carbon dioxide. The released SNO causes vasodilatation.

At the tissue level haemoglobin also picks up excess nitricoxide (NO), which tends to

cause vasoconstriction. Thus haemoglobin helps in regulating the blood pressure by

adjusting the amounts of SNO and NO to which blood vessels are exposed. This newly


22

appreciated role of haemoglobin bay influence development of drugs to treat

hypertension.

Further the arteriolar smooth muscle contraction can be increased by increased

sympathetic tone and also by increased sodium load and extra cellular fluid load.

The kidneys play an important role in the blood pressure regulation, and there is

considerable evidence that renal dysfunction is essential for the development and

maintenance of both essential and secondary hypertension.

The kidney influences both peripheral resistance and sodium homeostasis, and the

rennin-angiotensin system appears central to these influences. Rennin elaborated by the

juxtaglomerular cells of the kidney transforms plasma angiotensinogen to angiotensinI,

and the latter is converted to angiotensin II by angiotensin converting

enzyme(ACE).angtiotensin II alters blood pressure by increasing both peripheral

resistance and blood volume. The former effect is achieved largely by it’s ability tocause

vasoconstriction through indirect action on vascular smooth muscle, the latter by

stimulation of aldosterone secretion, which increases distal tubular re absorption of

sodium and thus of water.


23

Illustration showing the role of Renin-Angiotensin system:

JG

Renin

Renin substrate

Angiotensin I

Angiotensin II

Vaso constriction Increased Aldosterone systhesis

Sodium retention

BLOOD PRESSURE


24

The kidney produces a variety of vasodepressor or antihypertensive substances

that presumably counter balance the vasopressin effects of angiotensin. these

include the prostaglandins, a urinary kallikrein-kinin system, platelet-activating

factor, and nitric oxide.

When blood volume is reduced, the glomerular filtration rate falls(GFR), this ,in

turn, leads to increased reabsorption of sodium by proximal tubules in an attempt

to conserve sodium and expand blood volume.

GFR-independent natriuretic factors, including atrial natriureteic factor(ANF),a

peptide secreted by heart atria in response to volume expansion, inhibit sodium

reabsorption in distal tubules and cause vasodilation. Abnormalities in these renal

mechanisms are implicated in the pathogenesis of secondary hypertension in a

varietyu of renal diseases, but they also play an important role in essential

hypertension.


25

Measurement of blood pressure:The measurement of blood pressure should be done correctly. Blood pressure

varies from moment tomoment, respiration, emotion, exercise, meals, alchol, tobacco,

bladder distention, temperature and pain. It is also influenced by circadian rhythm, age

and race.

Shortly after “scopine-riva rocci” invented the sphygmomanometer the Russian

surgeon “korotkoff” suggested that by placing a stethoscope over the brachial artery at

the anticubitalfossa distal to the riva rocci cuff, sounds could be heard. The origin of

these sounds is still not clear, vibratory how phenomenon is probably responsible.

Blood pressure can be measured directly or indirectly. There are three common

devices used for the indirect measurement of blood pressure namely.

1. Sphygmomanometer, either mercury column or aneroid.

2. Electronic devices.

` 3. Automated ambulatory blood pressure devices.

However mercury sphygmomanometer remains the gold standard for

measurement.

The mercury column:

The mercury meniscus should be at zero.

The sphygmomanometer cuff:

Both the length and width of the inflatable bladder are critical. The bladder

(length) should encircle at least 80%of their circumference of the arm whilst the width

should at least b 40% of the circumference.

The sphygmomanometer inflation deflation device:

It is important to ensure that inflation deflation device functions properly.

The following may indicate malfunction of device.

*Failure to achieve a pressure of 40 mmof Hg above the estimated systolic blood pressure

or 200 mmoHg after 3-5 seconds of rapid inflation.

*The inability of the equipment of deflates slowly when the controlling release value is

opened at 2-3 mmofHg per second or at each pulse beat.


26

Auscultatory measurement of systolic and diastolic pressures:

The following technique is recommended for the measurement of blood pressure

using a sphygmomanometer:

Patient should be adequately rested seated with their arms supported and at heart

level. They should not have smoked or ingested coffee within 30 minutes of

measurement.

The systolic blood pressure should be estimated initially by palpation while

palpating the brachial/radial artery, the cuff is inflated until such time the pulse is no

longer palpable. The cuff should then be inflated to a further 30mmofHg. The cuff is then

slowly deflated and the pressure at which the pulse is palpable is estimated systolic blood

pressure.

The bladder is then inflated to 30 mmofHg above the previously estimated

systolic blood pressure and the pressure reduced at 2-3 mmofHg per second or pulse beat.

Here the auscultatory korotkoff sounds are classified under five phases.

Phase I:

The first appearance of faint clear tapping sounds (thuds) which gradually

increase in intensity. This gives the systolic blood pressure. This technique is important

because phase I sounds sometimes disappears as pressure is reduced and reappear at a

lover level (the auscultatory gap) resulting in under estimation of the systolic blood

pressure.

Phase II:

The softening of the sounds which may become Swissing or blowing.


27

Phase III:

The return of sharper softer sounds, which become crisper, but new fully regain

the intensity of phase I sounds. Neither phase II nor phase III has any known clinical

significance.

Phase IV:

Distinct abrupt muffling of sounds, which become soft and blowing.

Phase V:

The point at which all sounds disappear completely. This should be taken as the

diastolic reading.

In some groups eg: pregnant woman, anemia or elderly patents the sounds may

continue until the zero point. In such instances the muffling of the respective sounds

(korotkoff phase IV) is taken as the diastolic pressure. The point of muffling is usually

higher than the true arterial blood pressure. If korotkoff phase IV is used this should be

clearly recorded.

The blood pressure should be measured in both arms. It the difference in blood

pressure between the two arms is >20/10 mmofHg, then may be an anomaly which

requires further evaluation.

The blood pressure should be taken both lying and at least one minute after

standing to detect any postural drop.


28

Showing the phases of korotkoff sounds:


29

NIRUKTHI:

The word “Bhrama” dathu adding ghai pratyaya bhrama shabdha is derived. It is

pumlinga shabdha.

PARIBHASHA:

“Chakravath bhramato gatram bhoomou patati sarvadaa

Bhrama roga iti gneyo”

Bhrama defined as reeling sensation experienced by a patient forcing him to

losing his balance there by falling on ground.

Vertigo definition:(stedman’s dictionary)

A sensation of irregular or whisling motion either of oneself (subjective vertigo)

or of external objects (objective vertigo).

Implies a definite sensation of rotation of the subject or of objects about the

subject in any plane.

DEFINITION:The definition of hypertension has been revised by various authorities including

the world health organization/international society of hypertension(WHO/ISH) and the

American joint national committee on the detection, evaluation and treatment of high

blood pressure (JNC-VII report) and they define as any blood pressure reading that

Consistently stays at 140/90 or higher is considered higher blood pressure.

Desirable blood pressure for healthy adult is 120 Systolic Blood Pressure/80

Diastolic Blood Pressure.

Hypertension is the level of blood pressure at which the benefits of treatment

Outweigh its costs and hazards.

Definition of Essential hypertension:Hypertension is said to be essential when there is no obvious precipitating cause.


30

Traditionally the diagnostic level of essential hypertension is applied only to those cases

of hypertension where investigation has failed to reveal any renal, endocrine or other

primary cause. Unfortunately there is no clinical or laboratory tests which can provide a

quick positive diagnosis of essential hypertension and exclude other secondary types of

hypertension but, essential hypertension is a clinical entity in itself, although its

pathogenesis is unknown.

In more than 95%of people who have high blood pressure the underlying cause

is listed as essential hypertension. Thus, patients with arterial hypertension and no

definable cause are said to have primary, essential or idiopathic hypertension.

In recent times many Ayurvedic scholars have tried to give an appropriate term

to hypertension in Ayurveda. Following are the different correlations and different

terminologies suggested by various scholars-

Raktagata vata :Prof. Yadunandana Upadhyaya. And

Shri Sudarshana shatri; Bhupendra pal(varanasi)

Siragata vata :Prof.G.N.Chaturvedi and Dr.K.N.Shastri

Roudira mada :Acharya vishwanath dwivedi

Dhamani pratichaya : Vaidya A.D.Athawale; Vaidya Ranajit Rai Desai

Rakta vata :Prof.Yadunandana upadhyaya and

Sri Sudarshana shastri; Dr.sharma(Puri)

Dhamani upalepa :Prof.G.N.Chaturvedi and Dr.K.N.Shastri

Mada,Murcha,Sanyasa :Kaviraj kumud ranjan roy

Vyana bala vaishamya :Vaidya brihaspati Triguna

Dhamani prapoornata :Vaidya G.N.Saraswathi

Uccha rakta nipeedana :Acharya vidhyadar shukla

Uccha rakta bhara : Dr.Patak U.C.(Jaipur)

Rakta sammardhana :Prof.G.N.Chaturvedi

Rasa bhara :Vaidya T.S.Mishra

Avritha vata roga :Vaidya R.K.Sharma

Rakta sampeedana :Vaidya S.P.Panday


31

Rakta vega vriddi :Vaidya V.B.Athavale

Sleshmavrita vyana :Dr.Gupta H.C.(varanasi)

Raktatimardam :Dr.John K.George

Uccha rakta chapa :Prof.Madan gopal sharma and

Dr.Ajay kumar shrma

Prevalence:The prevalence of hypertension depends on both the racial composition of the

population studied and the criteria used to define the condition. In a elite suburban

population like that in the Framingham study merely 1/5th of individuals have high blood

pressure’s >160/95, while almost one half have pressures >140/90. An even higher

prevalence has been documented in the nonwhite population.

In females, the prevalence is closely related to age, with a substantial increasing

occurring after age 50. This increase presumably related to the hormonal changes of

menopause, although the mechanism is not clear.

Prevalence of various forms of hypertension in the general population and in

specialized referral clinics.

Diagnosis General population in% Speciality clinic in%

A.Essential hypertension. 92-94 65-85

B.Renal hypertension

i)parenchyma

ii)Reno vascular

2-3

1-2

4-5

4-16

C.Endocrinal hypertension

i)Primary aldosteronism

ii)Pheochromocytoma

iii)Oralcontraceptive pill

induced hypertension

0.3

<0.1

0.5-1

0.5-12

0.2

1-2

D.Miscellaneous 0.2 1

Some of the other forms of hypertension are :


32

*Borderline systolic hypertension: The diastolic blood pressure is normal and systolic

blood pressure is between 140 and 159 mmofHg.

*Isolated systolic hypertension: The systolic blood pressure is 160 mmofHg and above

and fluctuates from time to time high in the morning and low at night.

*Labile(transient) hypertension: The patient is hypertensive at one time and

normotensive at another time.

*Benign hypertension: Is moderate elevation of blood pressure and the rise is slow over

the years.

*Malignant hypertension: Hypertension is associated with complications like papilla

edema, retinal exudates haemorrhage. No absolute blood pressure level can be assigned

for this condition. However these patients usually have blood pressure around 200/140

mmofHg.

*Accelerated hypertension: Denotes a recent rise in blood pressure with retinal damage,

but without an papilla edema.

*White coat hypertension: Is a condition in which blood pressure is elevated in the

presence of a medical person but falls when the subject leaves the medical environment.


33

NIDANAM:

Nidana panchaka consists of nidana, purvarupa, rupa, upashayanupashaya and

samprapthi.

Nidana is the hetu for the disease which is the causative and aggravating

factor.Nidana may be vyadi janaka and vyadhi bodhaka1.

“Bhrama” is the symptom in many diseases. It is not mentioned as an individual

disease. Which is manifested due to prakopa of vata,pitta and rajo guna2.

Every disease is due to tridosha vaishamyata only3. In this disease individual dosha

prakopa karanas can aggravate the doshas and causes the disease.

Vata prakopa karanas can aggravate the vata dosha in the body, pitta prakopa

karanas can cause the pittadosha prakopa and causes bhrama which is the cause for fall

on the ground4.

For the understanding purposes nidana can be divided into four sub divisions they

are i) Aharaja

ii) Viharaja

iii) Panchakarmajanya

iv) Anyaja

VATA PRAKOPAKA NIDANA:

a) Aharaja:

1. Teekshana, laghu, sheeta guna aharas can cause the vata prakopa5 .

2. Anashana, Adyashana, Vishamashana, Vishamopacharam, Viruddahara sevana

can also cause vata prakopa6.

3.Sushkashaka,Vallura,Varakoddalaka,,Koradoosha,Shyamaka.Neevara,Mudgara,

Masura,Adhaki,Harenu,Kalaya Nishpava7.


34

b) Viharaja:

1. Ativyayama, Vegasandharana, Vyavaya, Jagarana, Bharaharana,

Gajaturagaradha padhaticharya8, Prapatana, Bhagnam.

c) Panchkarmajanya:

1. Vamana, Virechana, Shirovirechana atiyogas9

2. Doshatisravanam

3. Raktati sravanam.

d) Anyaja:

1. Abhighata, Unmada, Shoka, Vishama sharirasya.

2. Chinta, Rogatikarshana.

3. Marma gatam10

4. Gajashva shigrayanam

5. Atitrasaka11

6. Kama shoka bhayam leads to vata prakopa12.

PITTA PRAKOPA KARANAS:

a) Aharaja:

1. Ushna, amla, lavana, kshara, katurasa adhika bhojana can cause pitta prakopa.

2. Ajirna bhojana, Atisevitha bhojana can cause pitta aggravation13.

3. Tila, Atasi, Dadhi, Sura, Sukta, Aranaala and Kuluttha.

4. Dushtannam

5. Vidahi padartha sevana

6. Ahara vidahikala14

7. Ksharam15.


35

b) Viharaja:

1. Teekshan atapa sevana, Agni santapa can cause pitta prakopa.

2. Shrama, Krodham16.

c) Pancha karmajanya:

1. Vamana, Virechana and Nasyakarma atiyogam17.

2. Doshati sravanam.

3. Raktati sravanam.

d) Anyaja:

1. S harad ritu and varsha ritu(Pitta sanchaya)

2. Madyahnam

3. Stri prasangam

4. Bhayam18

5. Krodham19

6. Ashudda lohas20.


36

NIDANA REFERENCES:

1. Cha.samhita nidana.1/7 –chakra pani teeka

2. Madhava nidana-17/19

3. Cha. Samhita Su.-19/37

4. Madhava nidana-17/20

5. Cha.samhita Nidana-11/9

6. Cha.samhita Su.-26/86-87

7. Susrutha samhita Su.-21/19

8. Susrutha samhita Su.-21/19

9. Cha.samhita chi.-28/15-18

10. Cha.Samhita Su.21/27

11. Chikitsa kalika

12. Cha.sam.chi.-3/

13. Cha.sam.nid.-1/22

14. Susrutha sam. Su.-21/11 Ashtanga sangraha nidana-1/27

15. Astanga sangraha Nidana-17

16. Cha.Sam. Nidana-1/22

17. Cha.sam.Chi.-28/15-18

18. Susrutha samhita Sutra-21

19. Cha.sam.Chi.-3/

20. Astanga sangraha Su.-9/57.


37

ETIOLOGY:

Essential hypertension means that the cause of disease is not known; however in

recent years, experimental, epidemiological and therapeutic evidence seems to indicate

that essential hypertension is due to one or combination of etiological factors.

Its diverse hemodynamic and pathophysiologic derangements are unlikely to

result from a single cause. Heredity is a predisposing factor, but the exact mechanism is

unclear. Racial and environmental factors seem to act only in genetically susceptible

persons. So the factors responsible for the development of essential hypertension are-

1)Genetic factors:

The role of heredity in the etiology of essential hypertension has long been

suspected. The evidences in support are the familial aggregation, occurrence of

hypertension in twins, epidemiologic data, experimental animal studies and identification

of susceptibility gene (angiotensinogen gene).

Recent advances in genetic determination of human essential hypertension are

discussed by reviewing the candidate genes.

Acharya charaka while describing the genetic influence in disease says, at the

time conception, if the beeja (shukra or ovum), beeja (chrosome) or beeja bhaga

avaytava(genes) get vitiated, it is likely to travel in subsequent generations1.

Dalhana has also commented that beeja dushti does not mean whole dushti, but

there may be a dushti of a part of beeja, that is the organ developing from that particular

part are also defective or abnormal2.while classifying the diseases, acarya sushritha has

mentioned “adibala pravritta vyadhi” and is said to originate due to deformity of raja or

veerya of the parents at the time of conception3.


38

2)Racial and environmental factors:

Surveys in the U.S have revealed higher incidence of essential hypertension in

blacks than in whites. But in rural Africa hypertension is relatively rare, suggesting that

the high prevalence in the U.S is not because of the genetic tendency, rather, it might be

due to adaptation of western life style by American blacks.

There is a lot of controversy as to what are the important environmental factors.

One of the strongest bits of evidence showing that, the environment in which a person

lives affects his blood pressure.

3) Salt intake:

The environmental factor that has received the greatest attention is salt intake,

although not everyone with excessive salt intake develops hypertension, the cause of

special sensitivity to salt varies with primary aldosteronism, bilateral renal artery

stenosis, renal parenchymal disease etc.

Diets, which are high in sodium, are usually low in potassium. Potassium

supplements improve the effects of experimental hypertension, and found to lower blood

pressure of mild to moderate hypertensive. Potassium antagonizes the biological effects

of sodium and there by reduces blood pressure.

Excessive use lavana is described in charaka samhita as the cause of rakta vriddi

and leads to shonitaja roga4. Since rakta dhatu is one of the important dushya in the

etiopathogenesis of hypertension, it is given more importance. The symptoms of

shonitaja roga are similar to this essential hypertension. Again charaka has told that

lavana should not be consumed in excess and for longer duration5.when excessively used,

it produces fatigue, lassitude and weakness of body6, which the symptoms are usually

found in patients of hypertension.

In ashtanga sangraha, lavana is said to increase shareera kleda leading to

increased cardiac output, one of the responsible factor in regulation of blood pressure.


39

4)Obesity:

There is however an important confounding factor to be taken into account that

there is a strong link between excess body fat, blood pressure levels and prevalence of

hypertension. As obesity contributes to go blood lipid abnormalities and impaired glucose

tolerance; it has particular significance as a factor underlying the increased prevalence of

coronary artery disease in hypertensive patients. For every 10%increase in weight a rise

of 6.5mmof Hg in systolic pressure was observed in Framingham study.

Sushrutha has mentioned medoroga leads to vata vikara7. Commenting on above

verse Dalhana explained that vatavikara is produced due to medvrita marga. Apart from

this in astauninditiya adhyaya of charaka sutrasthana, acharya has described the

complications of sthoulya. Here the apakva medas when deposited in reasvaha srota, may

lead to dhamani pratichaya8 (atherosclerosis), which is the main factor responsible for

hypertension.

5)Stress:

Acutely stressful stimuli certainly raise blood pressure and may be more causative

in subjects who have familial hypertension. Sustained or repeated emotional stress(anger,

frustration, envy, hatred, fear and worry) causes arteriolar contraction through an

outpouring of norepinephrine from the sympathetic vasomotor nerve endings and

epinephrine from the adrenalomedulla. It is probable that some of these persons have

inherited abnormalities of increased reactivity of the sympathetic vasomotor nerve

endings and epinephrine from the adrenal medulla. It is probable that some of these

persons have inherited abnormalities of increased reactivity of the sympathetic nerve-

endings to emotional sensory stress, and or increased reactivity of their arteriolar smooth

muscle to norepinephrine and epinephrine.

In some persons, the blood pressure increases due to the presence of the doctor

(white coat hypertension).this is possibly due to the temporary emotional stress. The over


40

activity of he sympathetic nervous system has an important part to play in the

pathogenesis of hypertension.

In ayurveda sthana of manas is said to be related to shira and hridaya, which are

in turn related to prana and vyana vayu respectively, which have influence over function

of maintaining the blood pressure. So aggrevated vata will initiate the process of

hypertension9.

Acharya charaka while describing about srotas, has mentioned that rasavaha

srotas get deranged due to chinta or worries, which is the responsible srotas for rasarakta

sancharam.

Raja and tama are the doshas pertaining to the mind and the types of morbidity

caused by them are kama, krodha, lobha, moha, bhaya etc10., Acharya charaka has

advised to suppress these factors11,because they tend to elevate raja and tama gunas

which cause manodushti. This obnoxious state of mana produces manovikara with

involvement of samjanavaha or manovaha srotas12. Further chakrapani commenting on

srotomula says, hridya and dashadhamani are the manovaha srotomula13. In this way the

arteries of the heart may get afflicted by these manovikara and therefore they also afflict

oja which is also ashrita of hridaya14, and vitiation of vata and pitta15, also takes place.

Hence it may be concluded that all the psychological factors directly (vitiated vata

with involvement of hridaya, oja and dhamanies) provoke vyana vata, which can produce

hypertensive state.

Urban populations have higher blood pressures than rural populations. Further

the adverse effects of urban living are confirmed by the rise of blood pressure in the rural

population migrating to cities. Crowding, air pollution and stress in cities may be

responsible for this happening.


41

6)Meals:

After meals the blood pressure is little higher.

7)Emotions:

Rage and panic raise the blood pressure, however, in exceptional panic, there may

be fainting attacks.

8)Sleep:

Sleep causes a fall of blood pressure. However, sleep associated with nightmare,

dreams may cause rise of blood pressure.

9)Exposure to cold:

It causes rise of blood pressure. This is due to hypothalamic stimulation. There is

cutaneous vasoconstriction leading to increased resistance to the blood flow and elevation

of blood pressure (cutaneous vasoconstriction causes conservation of heat within the

body).

10)Geographic factors:

Several studies have shown that high altitude residents have lower blood pressure.

Possible constituting factors include-

1) Lower peripheral resistrance due to increased capillarisation of tissues.

2) Hypoxia causing reduced thyroid activity and

3) Primitive conditions.

11)Physical activity:

Several population studies have suggested that individuals who undertake regular

physical exercise have lower blood pressures than sedentary individuals.


42

Regarding exercises, dynamic exercise raises blood pressure and isometric

exercise raises it a lot more. Despite this, there is good evidence that people who take

regular exercises are healthier and have lower blood pressures than those who take none.

In Ayurveda idle sitting is told to be one of the astamaha doshakarabhava16

While moderate normal exercise brings about the healthy state of body and mind.

Therefore, lack of physical exercise for prolonged period may result in agnimandya.

Hence produce apakva ama rasa, which deposits in vahinis and produce dhamaniupalepa

or pratichaya. On the other hand, over exercise leads to vata prakopa, leading to

aggravation of vataja vyadhi.

12)Trace metals:

It has been claimed that both cadmium and lead; which are environmental

pollutants, may cause high blood pressure. The main source of cadmium to the human

body is cigarette smoke. Conversely, however, there is fairly good evidence that blood

pressures are lower in areas where the drinking water is hard (i.e, has higher calcium

content). The mechanisms for this are unknown.

13)Socio-economic status:

Blood pressure is consistently higher in people from the lower socio-economic

classes. The poorer classes have however, concurrently higher average body weight,

greater consumption of alcohol and tobacco and more exposure to noise etc., while some

studies in India have indicated a higher prevalence of hypertension in the higher socio-

economic groups, a very large study in Mumbai found no difference between high and

low socio-economic groups. So higher or lower socio-economic status does not have

significant effect on blood pressure.

14)Age:

The younger the patient when hypertension is first noted, the greater is the

reduction in life expectancy, if the hypertension is left untreated.


43

Older people tend to have higher blood pressure than young people. Almost all

surveys show that blood pressure rises with age in both men and women. Studies have

demonstrate the two important trends; firstly, blood pressure rises with advancing age

and secondly, those individuals whose blood pressure starts at a higher level tend to

retain their place in the distribution of blood pressure and therefore, sustain a faster age-

related rise in pressure. Due to thickening of vessel wall, as increase in sub-endothelial

layer and the media, which increase collagen content, elastic fragmentation and

calcification.

In vriddavasta vata is the predominant dosha.17 there is high predisposition to

develop vataja vikaras in the old age. Physiological aggravation of vata with it ruksha,

khara, daruna, sheeta gunas etc., may cause sankocha and kathinyata of the vessels.

15)Sex:

At all ages and in both whit and non-white populations, females with

hypertension fare better than males up to the age of 65,and the prevalence of

hypertension in pre menopausal females is substantially less than that in age matched

males or post menopausal women. Yet, compared with their normotensive counterparts,

females with hypertension run the same relative risk of a morbid cardiovascular event as

males do.

Regarding the less prevalence of hypertension in premenopausal females, the

possible explanation in ayurveda is that female body is purified every month because of

menopausal flow (in the context of prameha nidana).

16)Smoking:

Nicotine and carbon monoxide, two major products of tobacco combustion, are

both potent vasoconstrictors. Tobacco smoking has been reported to cause acute rise of

blood pressure, but whether prolonged smoking leads to sustained hypertension has not

been established. Several studies from the developed world have reported no relationship

between smoking and levels of blood pressure; some have even reported slightly lower


44

blood pressure amongst smoker’s .in the National study the percentage of smokers and

non-smokers was almost the same.

In Ayurveda, tobacco is derived from a plant Tamra (nicotiana tobacum), which

has the madaka effect and has property to aggravate pitta and rakta. It also causes

“bhrama” and mada. Apart from this, smoking causes rukshata in siras. Along with this

the deposition of nicotine causes narrowing of the lumen, thus vataprakopa and all

together resulting in to hypertension.

17)Alcohol intake:

Several studies have shown a strong and independent positive relationship

between alcohol intake and blood pressure. It has been estimated that about 10% of

hypertensives have alcohol-induced hypertension. The alcohol-hypertension relationship

still remains the subject of future research, particularly as no convincing mechanism can

yet be identified.

In Madatyaya chapter, acharya charaka has explained that, when madya is taken

in large quantity, it shall affect channels of rasa(rasavaha srotas)and by entering hridaya it

affect the dhatus situated in hridaya(rasa,oja,rakta). The gunas of alcohol like ushna,

teekshna, sukshma, vyavayi etc. are exactly opposite to the gunas of oja18,which also

provoke vata-pitta dosha. Destruction of oja would disrupt the normalcy of prana and

vyana vayu, sadhaka pitta and avalambaka kapha, which are the asritas of hridaya.

Charaka has also described pradusta, bahu (excessive), ushna, teekshna

madyapana and surapana as causative factors of shonita dushti. Further, It is the shelter

to moha, krodha, shoka and mrityu19 like wise madya affects dosha,dhatu,srotasadn

srotomula of rasavaha srotas(circulatory system) leading to hypertension20.


45

References:

1. Cha.sam.sha-3/17

2. Sushritha sam. Shar-4/36

3. Sushritha sam. Sutra-24/5


5. Cha.sam.Vima-1/15

6. Cha.sam.Vima-1/18

7. Sushrita sam.sutra-15/32

8. Cha.sam.sutra-21/4; Cha.sam.sutra-20/17; Asta.sam.Sutra-20

9. Asta.hri.sutra-12/4

10. Cha.sam.vima-6/5

11. Cha.sam.sutra-7/27

12. Cha.sam.sutra-24/25 chakrapani comment

13. Cha.sam.Indriya-5/41

14. Sushrita sam.sutra-15/23

15. Cha.sam.chi-28/16-17; Sushrita sam sutra-21/20

16. Cha.sam. siddi-12/11

17. Astanga hri.sutra-1/8

18. Cha.sam.chi.24/30-31; Sushrita sam utta-47/3

19. Cha.sam.chi-24/5

20. Cha.sam.chi-24/35-36


46

PURVA RUPA:Bhrama is a symptom which was mentioned in so many disorders.

Purva rupa is a symptom which describes or indicates the disease which is

appearing in the future1.

In some disorders the purvarupa may be seen in less quantity, further it may

increase when it reaches to rupavasta2,3.

Purvarupa can be divided into two types4. They are

1. Samanya purva rupa

2. Vishishta purva rupa.

In samanya purvarupa it indicates the disease but not the doshik dominance. But

in Vishishta purva rupa it indicates the disease as well as the doshik dominance of the

disease5.Bhrama mentioned as a purvarupa in the following disorders.

S.no. Name of the disease Mentioned in

1 Jwaram Cha.samhita

2 Apasmaram Cha.Samhita

3 Arshassu Susrutha samhita

4 Rakta pitta Ashtanga hridaya

5 Arshassu Astanga hridaya

6 Grahani Ashtanga hridaya

7 Kushta Ashtanga hridaya

8 Jwara(pitta) Madhava nidana

9 Masurika Madhava nidana

PURVA RUPA REFERENCES:1. Chakra datta commentary

2. Ashtanga sangraha Nidana-1/

3. Susrutha samhita Sutra.-21/

4. Madhu kosha comment

5. Madhu kosha comment.


47

RUPAM:The collection of symptoms which can indicate the present disease is known as

rupam1.

The symptoms of established disease are known as Rupas2.

The synonyms for the Rupam3 are 1.Samstanam

2. Vyanjanem

3. Lingam

4. Lakshanam

5. Chihnam

6. Akriti

The rupas can be devided into 2 types4.

They are 1. Samanya rupa

2. Vishishta rupa.

Vishishta rupa can also call as “Pratyatma lakshanam”/ “Pratyatmika lakshanam”.

Bhrama as a rupa mentioned in so many diseases by various authors.

These are In Jwara chapter VP Jwara, Sheeta jwara, Raktagata jwara, Antarvega

jwara and Pachyamana jwara by Madhavakara5.Whereas Charaka mentioned in Vata

Jwara and Pitta jwaraonly6. But Sushritha was not mentioned in Jwara chapter. Vagbhata

mentioned in VK Jwara, Visha jwara and Abhichara jwara7.

In other chapters the rupam bhrama mentioned as

Disease Author

1.Pittaja kasa8 Astanga hridaya nidana

2.Pittaja hridroga9 Astanga hridaya nidana

3.Vataja trishna10 Asta.Hri.Nidana

4.Vataja udavartha11 Madava nidana

5.Pittaja madatyayam 12,13 Asta.Hri.Nidana/Madava nidana

6.Vataja murcha14 Asta.Hri.Nidana

7.Pittaja chardi15 Madava nidana


48

8.Vataja arshas 16,17 Asta.Hri.Nidana/Madava nidana

9.Vata kundalika18 Asta.Hri.Nidana

10.Vata vidradi19 Asta.Hri.Nidana

11.Pittaja udaram/Sannipata udara 20,21 Asta.Hri.Nidana/Madava nidana

12.Pandu22 Asta.Hri.Nidana

13.Halimakam23 Madava nidana

14.Pittaja shopha 24,25 Asta.Hri.Nidana/Madava nidana

15.Agni,kardama,Grandi visarpa26 Astanga hridaya nidana

16.agni,kardama,grandi,sannipata visarpa27 Madavanidana

17.Raktagata vata/Mamsagata

medogata/Pittavrita vata/Pittavrita prana

vata/Pittavrita udana vata/PK yukta udana

vata28

Astanga hri.nidana/Sus.sam. nidana

18.Krimi29 Madavanidana

19.Marma kshata30 Madavanidana

20.Vataja amlapitta/Adogata amlapitta Madavanidana

21.Majjagata masurika Madavanidana

22.Rakta pradaram Madavanidana

23.Dushi visham Madavanidana

Rupam references:

1. Madhu kosha comment

2. Cha.Nidana-11/

3. Asta.Sam.Nidana-1

4. Chakrapani comment

5. Madava nidana –jwara chap.

6. Cha.Sam.Nidana-jwara chap.

7. Asta.hri.nidana-jwara chap.

8. Asta.hri.nidana-kasa chap


49

9. Asta.hri.nidana-hridroga chap

10. Asta.hri.nidana-Trishna chap.

11. Madava nidana-Udavartha chap.

12. Asta.hri.nidana-madatyaya chap.

13. Madava nidana-madatyaya chap

14. Asta.hri.nidana-murcha chap

15. Madava nidana-chardi chap

16. Asta.hri.nidana-arshas chap

17. Madava nidana-arshas chap

18. Asta.hri.nidana-

19. Asta.hri.nidana-vidradi chap

20. Asta.hri.nidana-udaram chap

21. Madava nidana-udaram chap

22. Asta.hri.nidana-pandu chap

23. Madava nidana-pandu chap

24. Asta.hri.nidana-shopha chap

25. Madava nidana-shopaha chap

26. Asta.hri.nidana-visarpa chap

27. Madava nidana-visarpa chap

28. Sushri.sam.Nidana-Vata vyadi chap.

29. Madava nidana-krimi chap


50

SAMPRAPTHI:Samprapthi is defined as the phenomenon of pathogenesis of a disease in a

healthy body.

The series of establishment of a disease and its exhibition of signs and symptoms

occurs in this process. Jati and Aagati1 are other synonyms for samprapthi.

The main event of samprapthi is “dosha dushya sammurchana”2.

I.SANCHAYA- Accumulation of dosha occurs

II.PRAKOPA- Vitiation of dosha occurs.

III.PRASARA- Spreading of the doshas in the body.

IV.STANA SAMSRAYAM- Dosha dushya sammurchana

V.VYAKTAVASTHA- Exhibition of signs and symptoms

VI.BHEDAVASTHA- Stage of complications.

I.SANCHAYAM:

Defined as accumulation of doshas in their respective places due to the nidana

factors3.

All the vata prakopaka ahara viharas cause sanchayam of vata and pitta prakopa

ahara viharas can sanchayam of pitta.

In bhrama the mahjor doshas are vata and pitta hence when teekshnadi pitta gunas

associated with sheetala guna cause sanchayam of pitta. Rukshadi vata gunas associated

with ushna guna causes sanchayam of vata4.


51

II.PRAKOPAVASTHA:

Aggravations of doshas in vilayana rupa are called prakopam5.

When vata, pitta are in sanchayavastha due to continuation of nidana factors the

doshas enters into prakopavastha. In this stage doshas are ready to dislodge from their

respective places.

For vata, dosha prakopa occurs in pravrit kala and varsha kaala when rukshadi

vata gunas associated with sheeta guna leads to vata prakopa6.

In sharath ritu pitta prakopa occurs and when teekshnadi pitta gunas associated

with ushna guna leads to pitta prakopa7.

III.PRASARAM:

When vata and pitta are in prakopavastha due to continuation oa vata ,pitta

prakopa ahara viharas and manasika karanas the doshas enters into prasaravastha. In this

stage doshas enters into the whole body or half of body or any part of the body and did a

place for the disease8.

If nidana continuous further that place becomes stana samsraya for the disease.

In “bhrama” aggravated vata,pitta doshas which are there in prakopavastha are

enters into prasaravastha and make the hridayam and sarva shariram as stana for the

disease which further leads to stana samsrayam.

Prakopavastha doshas may be enters into the prasarvastha due to following

reasons9.

1. Exercise

2. Excessive heat form internal/external

3. Teekshna ahara/vihara/oushadha

4. Ahita ahara viharas.


52

IV.STANA SAMSRAYAVASTHA:

When doshas are in prasaravastha,if nidana continuous they reach the stana

samsrayavastha. It is also called as “dosha dushya sammurchanavastha”.

Actually in this stage the purva rupas of the disease will be occurs and dosha

dushya sammurchana also stays in first stage due to this reason the lakshanas of the

disease are appears in mild form10.

In “bhrama” the lakshanas like reeling sensation experienced by a patient forcinghim to lose his balance there by falling on ground.

V.VYAKTIBHAVAM:

When doshas are in stana samsrayavastha, if patient was not treated properly then

doshas enters into vyaktibhavam. In this stage the symnptoms (rupam)appears very

clearly11. After formation of the rupas also if not given trteatment then sroto vaigunyam

occurs this associated with dathus or malas then dosha dushy sammurcha occurs. Then it

establishes as a disease. But, it is not possible to name every disease12.Treatment should

be given based on nidana karanas, doshas and adistana stanas of the doshas13.

In “bhrama” the major symptoms are reeling sensation experienced by a patient

forcing him to lose his balance there by falling on ground. Associated symptoms may

occurs like murcha, daham,shula and chardanam14.

VI.BHEDHAM:

After vyaktibhava avasta of the disease, if not treated then it becomes asadhyam15.

From sanchaya stage to bhedavasta stage the doshas becomes stronger, and then it

becomes hard to treat16.

“Bhrama” mentioned as a upadrava in gulma roga by charaka17and ajirnam,

vataraktam aamavatam, hridrogam by Madhavakara18. When bhrama occurs in

madatyaya rogi it becomes asadhyam19.


53

Samanya Samprapthi:

By the constant and prolonged indulgence in the nidanas tridosha get’s vitiated as

a result agnidushti occurs. Because of this the consumed food will not get digested and

ama is produced. Here gunataha and karmathaha vriddi of vata, dravataha vriddhi of pitta

and gunataha vriddhi of kapha takes place. These doshas combines with ama and

produces Sama dosha. The Sama doshas travel through rasayani and spreads into hridaya

and takes tiryagati and reaches shakhagra. Because of the Sama dosha kha vaigunya takes

place any where between the rasavaha srotomula hridaya and sarvasharira. The

khavaigunya may be due to dosha dushti produced by nidana sevana or due to sahaja

karana. At the site of khavaigunya the tridoshas get’s sammurchita with rasa, rakta,

mamsa and meda, as a result, there will be derangement of rasavha, raktavaha,

mamsavaha, medovaha and manovaha srotas. Here, after dosha dushya sammurchana

following sequelae takes place.

Role of vitiated vata:

Because of the vitiation of vata which is lodged in the blood vessels, the khara and

laghu guna causes katinya, leading to reduction in the elasticity; as a result of it

margavarodha is produced. This may be taken as arteriosclerosis. Even the age,

vriddhavastha, this is predominant of vata, comtributes to the pathology.

Because of the vitiation of vata which is lodged in hridaya, the chalana or

praspandana karma of vyana vayu, prayatna karma of udana vayu and dharana karma

of prana vayu will be impaired. Because of this there will be impairment in the

initiation of contraction and relaxation, conduction of impulses, as a result of which

the increased doshas alter the functions of hridaya and increases the heart rate and

contration and relaxation, there by increasing the cardiac out put.

When doshas get’s lodged in dhamani’s of vrikka, kleda samvahana is hampered thus

it adds to the blood volume resulting into increased cardiac output.

Role of vitiated Pitta:

By the Drava guna vriddi of pitta, the rakta vriddhi takes place due to

ashrayashrayi sambandha. Pitta is considered to have the identical qualities of that of


54

catacholamines. Since here the pitta vriddhi takes place, this can be attributed to increase

in catacholamines. Then, when found in increased level are liable to increase blood

pressure by increasing the peripheral resistance and cardiac output.

Role of vititated Kapha:

The picchila guna of kapha increases the viscosity of blood, which is also one of

the factors responsible in the mechanism of high blood pressure.

Role of Ama and Medas:

The singdha, picchila, guru etc, guna of ama, excessive medas and apakwa medas

(improperly converted fat) accumulates in the blood vessels causing narrowing of

lumen of blood vessels, leading to margavarodha. This can be taken as

hypercholestraemic condition of the plasma.

The increased medas can also cause mechanical compression over the blood

vessels from out side, which is also one of the factors for increased peripheral

resistance.

Role of Mamsa dhatu:

Ultimately hypertension in course of time produces thickening of the walls of

heart to cope up with increased function of it. This can be taken as cardiac hypertrophy

and this condition can be taken as adhimamsata which is the preliminary symptom of

mamsavaha srotodusti.

Thus a combined effect of all these pathological events, contribute to increased

peripheral resistance and increased cardiac output leading to hypertension.

At this stage the promonitory symptoms will arise, but here since it being a

vatavyadhi the purvarupa are said to avyakta and some vague symptoms like shiroshoola,

bhrama, anidra tec., may be seen with very mild intensity.

After this, the disease progresses and the complete manifestation of disease takes

place and as a result of these pathological events the signs like hypertension, bounding

pulse etc., are seen. And symptoms may or may not be present. If present, symptoms

comprises of bhrama, shirashula, anidra etc. Even at this stage, if the treatment is not


55

started, the further vitiation of doshas takes place and land up into complication or

upadrava. This depends on the sthana or the organ that gets affected i.e., when mastishka

is affected, the condition or diseases like ardita, pakshagatha etc., are produced,it causes

drishti mandya etc., and when hridaya is affected, it causes hridroga etc.,

SAMPRAPTHI GHATAKAS:1. Dosha- shariraka- vata- vyana, prana, udana

Pitta- pachaka, sadhaka

Kapha - avalambaka.

Manasika- rajas, tamas

2. Dushya- Rasa, Rakta, Mamsa, Medho, Majja

3. Sanchara stana- Hridayam, sarva shariram

4. Agni- jataragni, dhatwagni

5. Ama- Jataragnimandyajanya, dhatwagnimandyajanya

6. Srotas- Rasavaha, Raktavaha, Manovaha

7. Srotodushti prakara- Atipravritti, Sangam

8. Adhistana- Hridaya, Dhamanis

9. Udbhava stana- Amashaya, Pakwashaya

10. Rogamarga- Madhyama, Bahya

11. Vyaktha stanam- Sarvadaihika.


56

SCHEMATIC REPRESENTATION OF SAMPRAPTHI OFBHRAMA W.S.R.TO HYPERTENSION:

Continues indulgence in Nidana

Dosha prakopa

Agnimandhyam

Aamam

Saama doshas

Dosha prasara to Hridaya and Sarvasharira.

Dosha Dushya Sammurchana

Leads to folloing sequele

Vata Amam Medho Vata Pitta Rakta KaphaDushti.

Increased heartRate. Viscosity of blood.

Cardiac OutputBhrama

Blood volume

Peripheral resistance

Hypertension

Narrowing ofblood vessels.


57

CLASSIFICATION OF HYPERTENSION:

Hypertension can be classified in several ways.

1. Systolic and Diastolic hypertension

2. Essential and Secondary hypertension.

3. Intermittent and Established hypertension.

4. On the basis of Severity.

1.Systolic and diastolic hypertension:

Systolic and diastolic hypertension often coexists but when theyt donot ot the two

the diastolic hypertension has greater significance. However recent epideological studies

have shown that systolic hypertension alone does shorten life.

I.Renal:

1. Chronic pyelonephritis

2. Acute and chronic glomerulonehpritis

3. Polycystic renal disease

4. Renovascular stenosis or renal infarction

5. Most other severe renaldiseases (Arteriolarnephrosclerosis,diabetic

nephropathy)

6. Renin producing tumours.

II.Endocrine:

1. Oral contraceptives

2. Adrenocortical hyperfunction.

a. Cushing disease and syndrome.

b. Primary hyper aldosteronism.

c. Congenital or hereditary adrenogenital syndromes.

(17 α-hydroxylase and 11β-hydroxylase defects).

3. Pheochromocytoma.

4. Myxoedema.

5. Acromegaly.


58

III.Neurogenic:

1. Psychogenic

2. Diencephalic syndrome

3. Familial dysautonomia

4. Polyneuritis (acute porphyria/lead poisoning)

5. Increased intracranial pressure (acute)

6. Spinal cord section (acute)

IV.Miscellaneous:

1. Coarctation of aorta

2. Increased intravascular volume (excessive transfusion, polycythemiavera)

3. Polyarteritis nodosa

4. Hypercalcaemia

5. Medications eg: glucocorticoids, cyclosporine.

V.Unknown etiology:

1. Essential hypertension (>90% of all cases of hypertension)

2. Toxaemia of pregnancy

3. Acute intermittent porphyria.

2.Essential and Secondary hypertension:

Hypertension may be essential in the sense that it is primary or without known

cause or it maybe secondary disease of some other organ, such as the kidney, endocrine

gland, central nervous system or aorta.

3.Intermittent or established hypertension:

Hypertension may be intermittent (labile) or established (sustained):very often the

formed is merely an early stage of the later.

A commonly accepted classification would be the one adopted from the sixth

report of the joint national committee on detection, evaluation and the treatment of high

blood pressure (JNC VII) archives of internal medicine.


59

4.Classification of blood pressure on the basis of severity.

Classification Systolic blood pressure Diastolic blood pressure

Normal <120 <80

Prehypertension 120-139 80-89

Stage I 140-159 90-99

Stage II >160 >100

*Based on the average of ≥2 readings take at each of two or more visits after an initial

screening.

Note: Classification of blood pressure for adults aged 18 yr and older not taking anti

hypertension drugs and not actually ill. When systolic and diastolic pressures fall into

different categories, the higher category should be selected to classify the individual’s

blood pressure status.

Inclusion Criteria:

(Based on “International Classification of Diseases -10”)

Essential hypertension(Primary hypertension)

High blood pressure.

Hypertension- (arterial)(Benign)(Essential)(Malignant)(Primary)(Systemic).

Exclusion Criteria:

Involving vessels of brain

-Sub Arachnoid Haemarrhage

-Intra Cerebral Haemarrhage

-Non-traumatic intracranial haemarrhage

-Cerebral infarction

-Stroke

-Occlusion and stenosis


60


-Cardio Vascular diseases

-Cardio vascular diseases.

-Sequel of Cardio vascular diseases.

Involving vessels of Eye and Retinal disorders.

SAMPRAPTHI REFERENCES:

1. Asta.sam.nidana-1

2. Madhukosha –comment “dosheti kartavyatopalakshitam vyadi janma

samprapthi”

3. Asta.hri.sutra-12/1 “chayovriddi svadamneva pradweshovriddi hetushu viparita

gunnechacha”

4. Asta.hri.sutra-12

5. sus.sam.chi-33/ dalhana comment

6. Asta hri.sutra-12

7. cha.sam.sutra-6/

8. sus.sam.sutra-18/

9. Cha.sam.sutra-18

10. Cha.sam.chi-11

11. Madhava nidana-introduction

12. Cha sam.sutra-18

13. Cha.sam.sutra-18

14. Cha.sam.chi-28/220 or Sus.Sam.Nidana-1/35 or Asta.hri.nidana-16/42

15. Sus.sam.sutra-21

16. Sus.sam.sutra-21

17. Cha.sam nidana-gulma chap

18. Madhavanidana

19. Madhavanidana-madatyaya chap.


61

PATHOGENESIS OF ESSENTIAL HYPERTENSION:

The pathogenesis of essential hypertension is not completely understood;

therefore we will have to content with describing some of the theories of essential

hypertension.

Arterial hypertension occurs when changes develop, that alter the relation ship

between blood volume and total peripheral resistance. For many of the secondary forms

of hypertension, these factors are seasonably well understood, but for essential

hypertension, these factors are reasonably well understood, but for essential hypertension

it is till obscure.

It is currently believed that essential hypertension results from an imbalance

between the mechanisms controlling-

1. Sodium homeostatis.

2. The sympathetic nervous system.

3. The rennin-angiotensin-aldosterone system.

4. Circulating vasoconstricting and vasodilating agents.

5. Neurotransmitters.

6. Insulin resistance.

7. Cell membrane alterations.

8. Endothelial dysfunction.

1) Sodium Homeostasis:

Most authorities believe that impaired renal sodium excretion is one of the first

changes in the development of hypertension. Sodium retention is followed by an

expansion of blood volume and a subsequent increase in cardiac output.

Essential hypertension appears to be a pathological condition due to an alteration

in the transport system for sodium and potassium. This results in a rise in the extra-

cellular sodium ion concentration, thus leading to a disturbance of sodium homeostasis.


62

2) The Sympathetic Nervous system:

Most sympathetic nerve endings release a hormone called nor-epinephrine. This

causes vasoconstriction of arterioles in the skin and splanchnic area leading to a rise in

blood pressure.

Sympathetic over activity can rise blood pressure by a variety of mechanisms, by

a direct vasomotor effect, by central action on the brain or by acting in association with

the rennin-angiotensin system causing sodium retention by acting on the kidneys.

3) Renin-Angiotensin-Aldosterone Sysytem:

The rennin-angiotensin-aldosterone axis increases blood pressure by increased

formation of angiotensin, increased sympathetic output; and increased aldosterone

secretion. Aldosterone increases re absorption of sodium and excretion of potassium in

the the kidneys. The two important stimuli leading to the release of rennin are a reduction

in afferent arteriolar pressure and sodium depletion.

Angiotensin is a powerful vasoconstrictor and is therefore capable of producing

hypertension. Angiotensin-II also stimulates aldosterone secretion from the adrenals.

In brief, reduced renal perfusion pressure leads to the production of renin and angiotensin

and further to salt and water retention. Thus a vicious circle may be established.

4) Circulating vasopressor and Vasodilator agents:

Peripheral vascular resistance is controlled by vasoconstrictors and vasodilators.

There is some evidence at present that the altered activity of vasopressor and vasodilator

agents may be involved in the pathogenesis of essential hypertension. The circulating

vasopressor agents include angiotensin-I, catecholamine, thromboxane, leucotrienes and

endothelin-I. Recently a new group of vasoconstrictors, the endothelins has been

identified. Endothelin-I is a powerful vasoconstrictor.

Two of the most powerful vaso-active mediators, nitric oxide and endothelin have

been discovered recently and both occur within endothelial cells. Nitric oxide is the

principle physiological vasodilator while endothelin is the most important

vasoconstrictor.


63

The kidney produces circulating vasodilators or angiotensive substances such as

prostaglandins, a urinary kallikrein-kinin system and platelet activating factor.

Abnormalities in the production of vasodilators are implicated in the pathogenesis

of hypertension. Arterial natriuretic peptide (ANP) is another additional circulating

vasodilator factor which is involved in the regulation of sodium and water excretion and

therefore influences blood pressure. ANP hormone is secreted by specialized cells in the

cardiac atria in response to expanded blood volume. ANP binds to specific receptors in

the kidneys and increases the urinary excretion of sodium. The renin-angiotensin-

aldosterone system is opposed by ANP, a vasodiloator. ANP dilates blood vessels, and

therefore has antihypertensive properties. At present, the relation between plasma levels

of ANP and hypertension is not clear.

5) Neurotransmitters:

Neurotransmitters disturbance influences the development of essential

hypertension. Disturbance of neurotransmitters including acetylcholine, noradrenaline,

substance P, neuropeptide Y, serotonin, dopamine and encephalin play a role in the

pathogenesis of essential hypertension.

6) Insulin Resistance:

Insulin resistance and /or hyper insulinaemia have been suggested as being

responsible for the increased arterial pressure in some patients of hypertension.

Hyperinsulinaemia produces renal sodium retention and increases sympathetic activity.

Either or both of these effects could lead to an increase in arterial pressure.

7) Vascular Endothelium in Hypertension:

The endothelium produces vaso active substances that regulate vascular smooth

muscle function and structure. A functional or healthy endothelium maintains a balance

between opposing states; dilation versus vasoconstriction ect.. in the functional

endothelium, low level of nitric oxide(NO)is continuously released to keep the blood

vessel in the state of dilatation.


64

In the physiologic state, the endothelium maintains the vascular tone. Under patho

physiologic conditions, however, tissue cells of vaso constrictive substances such as

angiotensin II increase. Angiotensin II also stimulates the release of endothelin, the most

potent vasoconstrictor.

8) Leptin Link to Hypertension:

Leptin is one of the regulators of blood pressure. Persons with high leptin levels

have elevated diastolic blood pressure.

9) G.Protein:

A recent study suggests that mutations in G.Proteins can lead to essential

hypertension.


65

Table showing the hypothetical scheme for the pathogenesis of Essentialhypertension:

Genetic influences Environmental factors

Defects in renalsodium hemostasis

Inadequate sodiumexcretion

Salt and Waterretention

Plasma & ECFvolume

Cardiac Output

Vascularreactivity Vascular wall

thickness

Hypertension

Total peripheralresistance


66

PATHOLOGY:The adverse effects of long standing systemic hypertension principally involve

small arteries, and arterioles, the heart, kidneys, brain and retina. The primary vascular

changes can cause damage in the kidneys, brain and retina. Hence the pathological

lesions of systemic hypertension can be grouped under two broad categories;

A) Arterial and cardiac lesions.

B) Effects of arterial lesions on other organs.

Arterial and cardiac lesions:

Heart:

In systemic hypertension, the left ventricle has to deal with an increased

resistance against blood ejection. This results in development of marked hypertrophy in

order to cope with the increased work load. Cardiac hypertrophy is the result of increased

total peripheral resistance resulting in increased work over a long period of time.

Arteries:

Systemic hypertension affects the arterial wall partly physically and partly

through the action of chemicals released from the kidney and the nervous system. The

main effect of hypertension on large and medium arteries is the significant promotion of

the atherosclerosis, achieved primarily by injuring the endothelium and making it more

permeable to large atherogenic lipoprotein molecules.

Hypertension can affect small arteries and arterioles in any one or a combination of the

following three ways.

1. Hyaline (Benign) arteriosclerosis;

2. Hyperplastic arteriosclerosis;

3. Necrotizing arteriolitis or “Fibrinoid necrosis” of arterioles;

Hypertension can change a normal arteriole (A) in the following ways. It can

thicken its wall and diminish its lumen by inducing an insulation of plasma into the wall

(hyaline arteriolar sclerosis). It can thicken its wall and narrow the lumen by causing


67

proliferation of wall myocytes (“hyperplastic arteriolar sclerosis”). It can cause necrosis

of part or the whole wall (“necrotizing arteriolitis”); this can in turn induce hemorrhage.

or thrombosis.

Effects of Arterial Lesions on other organs:

Kidneys:(Hypertensive renal disease):

Changes in renal arterioles occur in most cases of hypertension. Microscopically

the afferent arterioles show necrotizing arteriolitis. Some small sized blood vessels also

show cellular hyperplasia (productive endarteritis),in which due to concentric cellular

hyperplasia, the wall looks like an onion skin.

Brain: (Hypertensive cerebral disease):

Hypertension adversely affects the brain in a variety of ways. In the brain,

malignant hypertension can produce a massive hemorrhage mostly due to the rupture of

several necrotic arterioles at a time, but sometimes also due to the rupture of the

distended and weekened wall of congenital arterial “berry aneurysma”.

In hypertensive encephalopathy, pathologically, the brain shows cerebral oedema

and petechial haemorrhages. Walls of small arteries and arterioles may snow fibrinoid

necrosis.

Idiopathic intracranialo hypertension (IIH), also known as pseudotumour cerebri is

characterized by increased intracranial pressure without enlarged ventricles or mass

lesions.

The pathophysiology of IIH is unknown. Elevated intracranial venous pressure has been

suggested as a universal mechanism in IIH of various etiologies. The only significant

complication of IIH is visual loss.


68

Retina: (Hypertensive retinopathy):

In the retina, the retinal arterioles show all the changes of hypertension on

fundoscopic examination. The changes due to severe hypertension are;

a) Hypoxia due to the thickened walls and narrowed lumen of arterioles, which an

fundoscopy look like “Silver wires”.

b) Patches of oedema due to the increased endothelial permeability of arerioles

and capillaries, and

c) Haemorrhages due to the rupture of several injured small vessel walls.

The clinical results of the above are visual disturbances ranging from blurring of

vision to complete blindness (Scotoma). Hypertensive retinopathy is classified according

to the severity of above lesions from Grade I-IV. More serious and severe changes with

poor prognosis occur in higher grades of hypertensive retinopathy.

Keith and Wagner’s Grading of Hypertensive Retinopathy:

Grade-I Thickening and tortuositry of arteries showing silver wiring appearance.

Grade-II Grade I changes plus arteriovenous nipping.

Grade-III Grade II changes plus flame shaped (superficial)haemorrhages and cottonwool

exudates.

Grade-IV Grade-III changes plus papilloedema.


69

DIFFERENTIAL DIAGNOSIS:In modern science essential hypertension should be differentiated from secondary

hypertension. Following are the differentiating features.

FACTORS ESSENTIAL HYPERTENSION SECONDARY

HYPERTENSION.

INCIDENCE 95% 5%

ETIOLOGY Unknown etiology Renaldiseases,renovasculardise

ases,renal neoplasms,

endocrine diseases, drug

induced etc.,

HISTORY A strong family history of

hypertension, along with reported

finding of intermittent pressure

elevation in the past favours the

diagnosis of essential hypertension.

Often develops before the age

of 35or after 55.history of use

of steroids or estrogens is of

obvious significance.

PATHOLOGY Pathogenesis is not clearly

understood and pathology pertains to

heart and blood vessels

Pathogenesis and pathology

depends on the disease that has

caused hypertension.

BLOOD

PRESSURE

RECORDING

A rise in diastolic pressure when the

patient goes from the supine to the

standing position is most compatible

with essential hypertension.

A fall in the absence of

antihypertensive medication

with the treatment of the cause,

suggest secondary forms of

hypertension.

SYMPTOMS Symptomatic or asymptomatic,

vague symptoms like headache,

bhrama, easy fatigability etc., will be

present.

Symptoms will be present with

the underlying disease.

INVESTIGATI

ONS

Urine analysis and

microscopy,serumurea,creatinine,uri

Depending on underlying the

disease, the values of these


70

cacid,serum electrolytes,fasting

glucose,fasting lipids,ECG and chest

X ray. The values of all laboratory

investigations will be within normal

range. ECG and chest X-ray will be

normal.

laboratory investigations and

ECG and chest X-ray varies.

Here some special studies are

needed to screen for secondary

hypertension.

PROGNOSIS It is controllable with proper

treatment. It requires life long

monitoring and treatment may

require periodic adjustments.

It is curable .when cause is

treated, the elevated blood

pressure comes down to

normal.

TREATMENT Treatment comprises of

1.Non drug therapy

Relief of stress

Dietary management

Regular aerobic exercise

Weight reduction

Control of other risk factors

2.Drug therapy

In general six classes of drugs are

used.

Diuretics

Antiadrenergic agents

Vasodilators

Calcium entry blockers

ACE Inhibitors and

Angiotensin receptors

antagonists

Treatment depends on the

cause and requires drug

therapy during severe

condition.


71

COMPLICATIONS:(UPADRAVAS)The occurrence of another disease in the wake of primary disease, as a

complication or sequel, is termed as upadrava (Madhukosha).

Sushritha while mentioning upadravas of mahagada, in which vata vyadhi is one

amongthem, explainspranakshaya, mamsakshaya, jwara, atisara, murcha, trishna, hikka,

shosha, chardi, shwasa. Dalhana commenting on this says some acharyas considers

shotha in place of shosha. So thus here shotha, shwasa i.e., edema and dyspnoes can be

taken as the complications. Most of the acharyas considers essential hypertension to that

of avrita vata rogas and even some lakshanas also correlates with avritha vata rogas.

Acharya charaka while explaining the upadravas of avritha vata rogas mentions Hridroga

as one of the complications.

In modern science the complications of essential hypertension can be classified on

the basis of –

Target organ damage

Atherosclerotic and pressure induced.


72

COMPLICATIONS OF ESSENTIAL HYPERTENSION:

ORGAN COMPLICATIONS

ATHEROSCLEROTIC PRESSURE INDUCED

BRAIN Cerebralinfarction,

Transient ischaemic

attacks

Hypertensiveencephalopathy,

Cerebral haemorrhage,

Lacunar infarcts

EYE Retinal vascular accidents Exudative and haemorrhagic

changes,Papilloedema.

HEART Angina,Myocardiac

infarction,Sudden death

Hypertensive heart disease, Left

ventricularhypertrophy,cardiomagaly,

ECGabnormalities,

congestive cardiac failure.

KIDNEY Renovascular disease Arteriolar nephrosclerosis,

Benign-without fibrinoid,

Malignant-with fibrinoid.

PERIPHERAL

ARTERIES

Intermittentclaudication,

Vascular occlusion.

Aneurysms, aortic dissection.


73

DIAGNOSIS AND ASSESSMENT:

Hypertension should not be diagnosed on the basis of the single measurement

unless there is target organ damage (TOD) or SBP-160-210 mm of Hg or DBP100-120

mm of Hg. Otherwise, the initial elevated readings should be conformed on at least 2

subsequent visits. The reevaluation may be done within days or weeks depending upon

the level of the initial blood pressure.

The objectives of evaluating a newly diagnosed hypertensive patient should be to

search for causes, define target organ status and look for other atherogenic risk factors.

A complete history should be taken. Symptoms of TOD as well as concomitant

conditions that increase morbidity and mortality such as diabetes, obesity and hyper

lipidaemia should be noted. A history of smoking, alcohol and sodium intake is also

relevant. In the family history, attention should be payed to the presence of hypertension,

diabetes, hyperlipidemia, ischaemic heart disease and stroke.

Secondary causes of hypertension should be excluded. These include renal

parenchymal disease, endocrine disorders, coarctation of the aorta and renovascular

hypertrension. A history of intake of oral contraceptives, non-steroidal anti-inflammatory

agents, steroids, nasal decongestants and liquorice should be enquired.

Physical examination should aim at assessing TOD, excluding secondary causes

of hypertension and identifying concomitant risk factors. These include:

General examination including height and weight.

Blood pressure measurement.

Carotid bruit, renal artery bruit and peripheral pulses.

Cardiac examination.

Respiratory examination.

Abdominal masses eg., polycystic kidneys.

Fundoscopy.

The initial workup should include the following investigations:


74

Urine analysis and microscopy.

Serum urea, creatinine, uricacid.

Serum electrolytes.

Fasting glucose

Fasting lipids.

Electrocardiogram (ECG) and chest X-ray.

If the examination or investigations suggest a secondary cause, the patient should

undergo special evaluation. If there is TOD further tests should be done to evaluate

the severity.


75

CHIKITSA:

Vyadhiharana kriyas are known as chikitsa1. Roga nidana pratikaras are also

called as chikitsa2. Sushritha mentioned as “nidana parivarjana” as a chikitsa3.

In every disease the nidana is compulsory to manifest the disease. Its parivarjana

itself becomes treatment for that disease.The treatment which is going to be done by

ahara, viharas and oushadha dravyas are called as “yuktivyapashraya chikitsa”4.

In “bhrama” the major doshas are vata and pitta. Vata and pitta hara ahara and

viharas and medhya dravyas are useful to treat the bhrama. “Bhrama” was mentioned in

“pittavrita prana vata” by charaka5 and vagbhata6.Charaka mentioned treatment for

“pittavrita vata” in his chikitsa stana7.

He mentioned that ushna rupa chikitsa and sheeta rupa chikitsa should be done in

alternatively until the lakshanas subside.Jeevaniya gana dravya grita indicated for this.He

mentioned Jangala jantu mamsam, yava,shali as a aharas for pittavrita vata. Yapana vastis

and ksheera vastis are also mentioned8.

REFERENCES:

1. Vaidyaka shabha sindhu-“ya kriya vyadhi harani saa chikits nigadyate”

2. Vaidyaka shabha sindhu-“chikitsa roga nidana pratikara”

3. Sus.sam.Uttara-1/25

4. Cha.sam.sutra-21

5. Cha.sam.chi.-28/220

6. Asta.hri.nidana-16/42

7. Cha.sam.chi-28/184

8. Cha.sam.chi-28/185.


76

TREATMENT:

Hypertension is highly prevalent and powerful contributor to cardiovascular

morbidity and mortality in the general population. The high prevalence of this condition

continues despite the introduction of increasingly effective number of anti-hypertensive

agents. It is blood pressure that kills hypertensives, not hypertension.

Once diagnosed, hypertension requires on going management, despite the absence

of symptoms. The goal of treatment in patients with hypertension is to prevent morbidity

and mortality associated with high blood pressure by least intrusive means possible. The

benefits of treatment have to be weighed against side effects and inconvenience, so it is

important to treat the whole patient, not just the blood pressure. This can be to a large

extent accomplished by achieving and maintaining SBP<140 mm of Hg and

DBP<90mmofHg with the most cost effective means while maintaining good quality of

life.

Treatment of blood pressure encompasses non-pharmacological and

pharmacological measures. Non-pharmacological intervention through life style

modification is advocated as initial therapy for essential hypertension.

Non-Pharmacological Management includes:

Relief of emotional and environmental stress.

Sodium intake: Elderly people are more sensitive to sodium intake. An

intake<100 m mol or 6 gm sodium chloride a day us recommended.

Weight reduction: weight reduction is most beneficial in patients who are more

than 10% over weight. As far as possible, aim for ideal Body Mass Index(BMI)of

20-25 kg/m2.however even a 5%reduction in weight will result in significant

lowering of blood pressure.


77

Avoidance of excessive alcohol intake: the intake should not exceed 21 units per

week for men and 14 units per week for women. One unit of alcohol is equivalent

to ½ a pint of beer or 100ml of wine or 20ml of proof whisky.

Reduction of cholesterol and saturated fat intake: as with smoking, this is

important in reducing cardiovascular risk.

Regular physical exercise: dynamic isotonic exercise(eg., Jogging, walking.,) is

more effective than static isometric exercise(eg., weight lifting). Milder exercises

like brisk walking for 30-60minutes 3-5 times a week is preferred.

Cessation of smoking: This is important in the overall management of the

hypertensive patient in reducing cardiovascular risk.

Other non-pharmacological management includes micronutrient alterations and

dietary supplementation with fish oil, potassium, calcium, magnesium and fiber.

However they have limited or unproven efficacy.

TREATMENT INTERVENTION B.P.REDCUTION(mmofHg.)

Sodium restriction Dietary advice sodium

intake(<100m mols/day)

8-15 systolic

5-6 diastolic

Relaxation Relaxation techniques 9-27 systolic

4-16 diastolic

Weight loss Diet and exercise 9-27 mean arterial pressure

Exercise Aerobic exercise

programme

6-13systolic

9-12 diastolic.


78

Table showing initiation of modern treatment in patients withhypertension.

SBP 140-180 (or) DBP 90-110 mmofHg.

Assess other risk factors TOD

Initiate life style mesures

Stratify absolute risk

Veryhigh High Medium Low

Begin withDrug

Begin withDrug

Monitor BP&Other riskfactors for 3-6months

Monitor BP &Other riskfactors for 6-12months

SBP≥140 orDBP≥90 BeginDrug.

SBP≤140 orDBP≤90Continue toMonitor

SBP ≥150orDBP ≥95Begin Drug.

SBP ≤150DBP ≤95Continue toMonitor


79

Pharmacological management:

If non-pharmacological treatment does not succeed during 4-6 month period or if

the level of blood pressure is high, immediate antihypertensive drug therapy should be

implemented.

Approach to drug therapy:

The aim of drug therapy is to use the agents just described, alone or in

combination to return arterial pressure to normal levels with minimal side effects.

General principles:

1. Start with a low dose of an agent and, if blood pressure is not controlled, increase only

moderately.

2. Star with an agent that may also treat and /or not harm a coexisting condition.

3. Add a second agent from a different, complementary class if blood pressure is not

controlled with a moderate dose of the first agent.

4. Start with an agent that the patient is likely to tolerate best; long term compliance is

related to tolerability and efficacy of the first agent used.

5. Use a diuretic when two agents are used, in nearly all cases.

6. Use thiazide diuretic only at low doses,i.e, ≤25 mg/d of hydrochlorothiazide or its

equivalent, unless some pressing reason exists.

7. Use low dose combination therapy when appropriate as initial therapy;

a) A diuretic with a beta blocker, ACE inhibitor or a beta blocker.

b) A calcium channel blocker with an ACE inhibitor or a beta blocker.

8. One or two agents will control blood pressure in 90% of hypertensive patients.

If therapy with two drugs does not achieve blood pressure control, the primary

agent should be increased to full dose. If the blood pressure is still not controlled, then a

detailed search for a secondary cause of hypertension is indicated. If none is found, then a


80

dietary assessment will often reveal a high sodium intake. With reduction in salt intake ti

5gm/day or less, blood pressure is often controlled.

If the blood pressure is controlled, then a stepwise reduction in the and /or with

drawl of some of the agents should be carried out to determine the minimal therapeutic

programme that will maintain the blood pressure at 140/90mmofHg or less. Whether

triple or quadruple drug therapy is warranted to lower blood pressure, further is uncertain.

In general, there are sex classes of drugs; diuretics, anti adrenergic agents,

vasodilators, calcium entry blockers, angiotensin converting enzyme (ACE)inhibitors and

angiotensin receptor antagonists.


81

CLASS

OF

DRUG

COMPELLING

INDICATIONS

POSSIBLE

INDICATIONS

COMPELLING

CONTRA

INDICATIONS

POSSIBLE

CONTRA

INDICATIONS

DIURE

TICS

Heart failure,

elderly patients,

systolic

hypertension.

Diabetes Gout Dyslipidemia,

sexually active

males

Β-

BLOCKE

RS

Angina, after

myocardial

infarct,

tachyarrhythmias

Heart failure,

pregnancy,

diabetes

Asthma, COPD,

heart block.

Dyslipidemia,

athletes

&physically active

patients, peripheral

vascular disease

ACE INHI

BITORS

Heart failure,

LVF, after

myocardial

infarct, diabetic

nephropathy.

Pregnancy,

hyperkalaemabi

lateral renal

artery stenosis.

CALCIM

ANTA

GONISTS

Angina, elderly

patients, systolic

hypertension

Peripheral

vascular disease

Heart block Congestive heart

failure

Α-BLOCK

ERS

Prostatic

hypertrophy

Glucose

intolerance,

dyslipidemia

Orthostatic

hypotension.

ANGIOTE

NSIN II

ANTAGO

NISTS

ACE-inhibitor

cough.

Heart failure Pregnancy,hype

rkalaemia,

bilateral renal

artery stenosis.


82

PATHYAPATHYA:

In the treatment of the diseases, Pathyapathyas are given equal importance with

drugs, diet and therapeutic measures.

The pathyapathya that can be recommended on the basis of dosha dushyadi are as

follows.

Table showing the pathyapathya in Hypertension(Bhrama):

PATHYA APATHYA

AHARA Mudga,masoora,yava,palaka,

methica,jambeera,carrot,papaya,

drygrapes,orange,ardraka,rasona,

hingu,jeeraka,maricha,

jangala pakshi mamsa,godugda,

ajadugdha,takra etc.,

Anupa desha pakshimamsa,

dadhi,dugda vikara,tobacco,tea,

coffee,salt,fatty substances,

alcohol,etc.,

VIHARA Samyakvishrama,upavasa,shavasaa,

samyak vyayama,sadvrittapalana,

nitya abhyanga,Krodha-irsha-bhaya-

chinta-shokadi dharaniya vega

dharana,etc.,

Diasvapna,ativyayama,avyayama,

vegadharana,adhyashana,

atichintana,atikrodha,atishrama,

atisukhasana,ratrijagarana etc.,


83

CRITIRIA FOR THE SELECTION OF THE DRUGS:

The present compound used in the clinical trial is a combination of individual

drugs taken from “Bhavaprakasha nighantu”. This is named as “Karpasa Beejadi Gritha

Gutika”. This is anubhutha yoga.

All the drugs have vata, pitta hara and medhya properties. All the drugs are easily

available, non controversial and economical.

The disease “Bhrama”basically is a vaata, pitta predominant disease hence this

compound shall effectively counter the effects of vitiated vaata, pitas. As it also has

mehdhya property, it enhances the intellectual capacity of the brain.

This compound drug having the properties of madhura, tikta, kashaya rasas, guru

snigdha gunas, Sheeta virya and madhura vipaka predominantly. Due to Madhura, Tikta,

Kashaya rasa it acts as vata pitta shamaka. Almost all the drugs are having the medhya

property which is useful for enchance the intellectual capacity as well as acts as

anxyiolytic.

Guduchi is an immunomodulator, tridosha shamaka and medhya rasayana.

Aparajitha has a property of tridoshahara and medhya. Shatavari is a vata pitta hara drug

and Rasayana. Jatamansi is a tridoshahara and medhya. Karpasa beeja has a property of

VP hara and vrishya.

Gogritha is the only bhavana dravya for this compound. This is having the

madhura rasa, guru guna, sheeta virya and madhura vipaka. It is also a nitya rasayana. It

is vatapitta haram and Medhagnivardakam.Go gritham increases the HDL-cholesterol

levels and hence it is cardioprotective.


84

Description of individual drugs:

1.GUDUCHI:

Botanical name : Tinospora cordifolia

Family : Menispermaceae

Synonyms : amritha, avyatha, amritavalli, guduchika,

gundra,chakrangi,kundali

Properties:

RASA : Tikta, Kashaya

GUNA : Guru, Snigdha

VIRYA : Ushna

VIPAKA : Madhura

KARMA : Tridoshashamaka, medhya, rasaya, dipaniya, grahi,

Medhohara, kandgna, jwarahara, dahaprashamana.

PARTS USED: Stem, root, areal roots

DOSE : Stem powder: 3-6 gm

Decoction: 50-100ml

Fresh juice: 10-20ml

Guduchi satva: 1-2 gm

Chemical constituents: A diterpine of columbin type-tinosporin is isolated from

plant.

Tinosporidine and beta sitosterol isolated from stems. Cordifor, heptacosanor and

octacosanol reported from the leaves. A new furanoid diterpine-tinosporide from

stems.18-norclerodene glucoise-tinosporaside from stem wood is reported.

Iso columbin, tetra hydropalmatine, magnoflarine and palmatine were isolated

from roots.It is mentioned in Hridroga by vanga sena1.


85

References:

1. Vanga sena- vata vyadhi prakarana

2. Bhava prakasha nighantu-3/1-10.

3. Dhanvantari nghantu 1/1-4,

4. Shodhala nighantu-1/96-98.

5. Cha.sam.Sutra-25/

Guduchi:

“Rasoguduchyaasthu samula pushpyah kalka prayojyah khalu shankha pushpyah

Aayuh pradhaanyamaya nashanaani balagni varna swara vardhanaani,

Medhyaani chaitani rasaayani medhyani vishesheenacha shankhapushpee”

(Cha.Sam.Chi.1.3.30-31)

2.APARAAJITHA:Botanical name : Clitoria ternate

Family : Fabaceae

Synonyms : Aspotha, Gririkarni,Vishnukrantha, Swetha, Mahaswetha.

Properties:

RASA : Katu, Tikta, Kashaya

GUNA : Laghu, Ruksha

VIRYA : Sheeta

VIPAKA : Katu

KARMA : Tridosha hara, medhya, vishagna, chakshushya.

INDICATIONS : Kushta, shotha, unmada, vrana, shula.

PARTS USED : Root/Root bark; Seeds

DOSAGE : Root powder: 1-3gm.

Seed powder: 1-2gm.

Chemical constituents:

Aparajitin,tetraxerol,taraseron,alphaandbetasitosterols,robinin,quercitin,kaempfer

ol,ternatines A,B,C,D.It was mentioned in manasika rogas by raja marthanda.


86

References:

1. Bhava prakasha nighantu.

2. Raja marthanda.

“Aparaajithe medhye sheete kantye sudrishtide

Kushtamutra tridoshaama shotha vrana vishaapahe,

Kashaye katuke paake tikte cha smriti budhdhide”

(Bhava prakasha.)

3.SHATAVARI:Botanical name : Asparagus racemosus.

Family : Liliaceae

Synonyms : Indivara, Bahusuta,Madabanjini,Satamuli,

Sheetavirya,Atirasa.

Properties:

RASA : Madhura, Tikta

GUNA : Guru, Snigdha

VIRYA : Sheeta

VIPAKA : Madhura

KARMA : VP hara, Rasayana, Vrishya, Stanya janana.

INDICATIONS : Stanyakshaya, Artavakshaya, Raktapitta,Arshas,

Atisaara, Grahani, Kshaya, Gulma.

PARTS USED : Tuberous roots

DOSAGE : Fresh juice: 10-20ml.

Decoction: 50-100ml.

Powder: 3-6gm.


From roots: Sarasapogenin,two spirostanolic and two furostanolic

sponins,sitosterol,asparaganine A.


87

From fruits: beta-sitosterol, sarasapogenin, diosenin, Asparanins A and B.

From leaves: Favonoids, rutin.

The glycosidal fraction (0.5mg) of the plant produced bradycardia and reduction

in the force of contration.

A high dose (60mg/kg) produced a fall in blood pressure and depression of the

respiration of cat.(Roy et al., 1968,1971).

References:


“Medhaagni pushtidha snigdha netrya gulmaatisarajit

Shukrastanya kari balyaa vatapittasra shotha jit”

4.JATAMAMSI:Botanical name : Nardostachys jatamamsi

Family : Valeianaceae

Synonyms : Tapaswini,Nalada,Bhutajata,Vilomasha,Jata, Mamsi,Mura.

Properties:

RASA : Tikta, Kashaya, Madhura

GUNA : Laghu, Snigdha

VIRYA : Sheeta

VIPAKA : Katu.

KARMA : Tridoshahara, Medhya, Balya, Kushtagna.

INDICATIONS : Kushta, Kandu, Visarpa, Jvara, Daha.

PARTS USED : Rhizome.

DOSE : powder: 1-3 gm.


88


Actinidine,carotene,aristolens,calarene,elerid,droaristolene,bendesmol,JatamolsA

andB,Jatamansicacid,Jatamansone,Nardol,Nardostachonol,Nardostachone,Jatamansin,Jat

amansinol,Oroselol.

Research:

1. The essential oil from the rhizomes has a depressant action on the CNS of guinea pigs

and rats. (Chopra et al., 1954).

2.Thi oil free aquous extract showed a transient hypotensive effect and ECG changes in

dogs heart, apart from contracting frogs rectus muscle.The CVS effect of the extract was

similar to that of potassium.(sheth and kekra., 1956).

3. The alkaloid fraction showed a significant and sustained hypotensive action in dogs.

(Dose et al., 1957b).

4. Root powder showed a sedative action in a clinical study on 24 medical students as

evidenced by the prolongation of the visual reaction time. (Amin et al., 1961).

“Mamse tiktaa kashayaacha medhyaa kanti bala prada

Swadvee himaa tridoshaasra daha visarpa kushtanuth”

(Bhava prakasha)

5.KARPAASA BEEJA:Botanical name : Gossypium herbacium.

Family : Malvaceae

Synonyms : Tundikeri, swadanshtra.

Properties:

RASA : Katu

GUNA : Tikshna, Snigdha (Root bark-Laghu)

VIRYA : ushna

VIPAKA : Katu


89

KARMA : VP hara, Seed-vrishya, Leaf-mutrala, stanya janana.

INDICATIONS : Karna puya, karnanada, mutrakrichcha, anartava, kashtartava.

PARTS USED : Root, Flower, Seed.

DOSE : Decoction: 50-100ml;

Seed powder: 3-6 gm.


Root : hemigosypol;

Flowers : quercimetitrin;

Seed : gossypol;

Essential oil : caryophyllene, Pinene, Limonene.

References:


“Karpasako …….tatbheejam syandham vrishyam snigdham kaphakaram guru”

Toxic effects of G.Herbacium1:

Especially the root bark and seeds are used in medicine.

Constituents:

Cotton seed meal contains from 0.0059 to 0.053% of phenolic compound named

gossypol. Some times it produces toxic effects. It is due to presence of gossypol. This

acts as a capillary poison resulting in local inflammation and edema.

Symptoms of slow poisoning by feeding experimental animals with cotton seed

meal consist of diarrhea, loss of appetite, emaciations, edema of lings, shortness of

breath, neuritis, paralysis.

The disturbances of digestion and nutrition are due to enteritis.

Recent investigation shows that cotton seed meal poisonings in pigs is probably

not due to a toxic substance in the cotton seed meal but is brought to a greater or lesser

degree from iron deficiency in an ill balanced diet.

Iron in the shape of ferric oxide appears to have an especially beneficial effect in

preventing the onset of symptoms2.


90

References:

1. Poisonous plants of India by chopra (ICAR).

2. Mc Gowan and Crichton: Biochemistry ., 1924,18,273.

6.GO GRITHAM:Ghee is obtained by clarification of milk fat at high temperature, Ghee is almost

anhydrous milk fat and there is no similar product in other countries. Cow milk

constitutes carotenoids due to this its colour is golden yellow colour. Because of its

pleasing flavour and aroma, ghee has always had a supreme status as an indigenous

product in India.

Properties:

RASA : Madhura

GUNA : Guru

VIRYA : Sheeta

VIPAKA : Madhura

KARMA : Rasayam, Vata pitta haram, Swaryam, Varnyam

Physiochemical characteristics:

Chemically, ghee is a complex lipid of glycerides(usually mixed),free fatty

acids,phospholipids,sterols,sterol esters,fat soluble vitamins, carbonyls, hydrocarbons,

carotenoids ,small amounts of charred casein and traces of calium,phosphorus,iron,etc. It

contains not more than 0.3% moisture,glycerides constitutes about 98% of the total

material,of the remaining constituets of about 2%sterols(mostly cholesterols)occur to the

extent of about 0.5%. Ghee has a melting range of 280 to 440 C.

Cow ghee can bond with lipid-soluble nutrients and herbs to penetrate the lipid

based cell walls of the body. This way it can transport the active components to the


91

interior of the cell where they impart the most benefit. This was mentioned in ayurveda as

Yogavahi.

Ghee made purely from Cows milk contains beta carotene, Vitamin E,rich source

of vitamin A,and vitamin D.It also contains butyric acid and fatty acid with antiviral and

anticancer properties.

“Gritham pittaanila haram rasa sukraoujasaam hitam

Nirvaapanam mridukam svaravarn prasaadanam”

(Charaka samhita Sutra.-13/14)

“Vatapitta prakritayo vatapittavikarinah

Chakshushkamaah kshataah ksheenah vriddhah balaasthatah balaah

Ayu prakarsha kamascha balavarna svararthinah

Pushtikamaah prajakamah soukumaryarthinachayo

Deeptoujasmriti medhaagni buddhindriya balaarthina

Pibeyusarpirarthascha daha shastra vishaagnibhih”

(“Charaka samhita Sutra-13/42-43)


92

PICTURES OF INDIVIDUAL DRUGS:

GUDUCHI APARAJITHA

SHATAVARI JATAMAMSI

KARPASAGO GRITHAM


93

“KARPAASA BEEJADI GRITHA GUTIKA”:

KARPASABEEJADI GRITHA GUTIKA KARPASABEEJADI GRITHA GUTIKA

KARPASA BEEJAMKARPASA BEEJAM SECTION CUTTING


94

MODE OF PREPARATION OF COMPOUND DRUG:The compound prepared as a gutika/vati for the convience of the patient. This

Compound contains Guduchi, Aparajitha, Shatavari, Jatamamsi, Karpasa beejam and

“Go gritham”.

Guduchi, Aparajitha taken in the form of panchangam, Shatavari roots, Jatamamsi

Rhizome and Karpasa seeds were took for the preparation of the compound.

Guduchi and Aparajitha were dried in shadow area of the open air and made into

A fine powder. Shatavari roots, Jatamamsi rhizome and Karpasa seeds are made into a

fine powders by filtering through a cloth. All the powders are mixed in one vessel and Go

Gritha bhavana given one time and make it in to a pill of 500mg.

DOSAGE SCHEDULE:

Dosage schedule decided as 2 tablets (500mg each tablet), three times per a day

up to 45 days. Water used as an anupana for the intaking of the medicine.

RESTRICTIONS:

Each and every patient who undergone a trial for this drug are restricted not to

take excessive salt intake and other food items like pickles, papads, hot and spicy

Biryanis, fishes and eggs etc., and also advised for brisk walking for 40 min. daily.


95

CLINICAL STUDY:My clinical study is “The effect of Karpasa beejadi Gritha Gutika” in the

management of Bhrama with special reference of Hypertension”.

This comprises the following:

1. Method and Material.

2. Observations and Result.

1.Method:

Thirty cases of adult patients with giddiness (Bhrama) and essential hypertension

were studied for clinical trial from the kaya chikitsa I.P.D and OPD at the post graduate

training and research department and Govt.Ayurvedic Hospital.

In this trial patients suffering from heart failure, malignant hypertension and

suffering from any other serious complications were excluded. However patients

suffering from pakshagatha were included in this study. The patients were examined

daily and the blood pressure was recorded with the help of a standard

sphygmomanometer.

In all the cases routine investigations of

1. CBP

2. CUE

3. Examination of blood urea, serum creatinine and blood sugar were conducted to the

extent possible.

The signs and symptoms, and the general condition of the patient before

commencement of treatment and the improvement noted daily/weekly (for O.P.patients)

was recorded. The bhrama condition was observed throughout the course, along with

headache, sleeplessness and fall on the ground. Grading was given for Bhrama, Headache

and Sleeplessness these gradings are observed from schedule initiation to end of the

schedule, for the convenience of the subjective parameter result assessment i.e.,

symptomatic relief in bhrama, headache and sleeplessness.


96

These symptoms are graded as follows

Bhrama:

Grade 0-No giddiness

Grade 1-Postural giddiness

Grade 2-Moderate giddiness

Grade 3-Severe giddiness

Headache:

Grade 0-No headache

Grade 1-Slight headache

Grade 2-Bearable headache

Grade 3-Unbearable headache

Sleeplessness:

Grade 0-Sound sleep

Grade 1-Mild Sleep

Grade 2-Moderate sleep

Grade 3- No Sleep.

In the schedule initiation, according to these gradings the symptoms are noted

along with other signs and symptoms. After completion of the trial again the general

condition along with these symptoms are noted and compared with the initial symptoms

and grading.

The improvement in the subjective symptoms is divided into four categories.

They are Mild improvement, Moderate improvement, Marked improvement and No

response. When patient response was less than 35% it was grouped into no response

category, if response is between 35%-50% it was grouped into mild response category, if

response is in between 50%-75% it was grouped into moderate category and if response

is greater than 75% it was grouped into Marked improvement category.


97

Inclusion Criteria:

(Based on “International Classification of Diseases -10”)

Essential hypertension(Primary hypertension)

High blood pressure.

Hypertension- (arterial)(Benign)(Essential)(Malignant)(Primary)(Systemic).

Exclusion Criteria:

Involving vessels of brain

-Sub Arachnoid Haemarrhage

-Intra Cerebral Haemarrhage

-Non-traumatic intracranial haemarrhage

-Cerebral infarction

-Stroke



-Cardio Vascular diseases

-Cardio vascular diseases.

-Sequel of Cardio vascular diseases.

Involving vessels of Eye and Retinal disorders.


98

2.Material:

“Karpasa Beejadi Gritha Gutika” was used in this trial which contains

Guduchi, Aparajitha, Shatavari, Jatgamamsi, Karpasa beeja and Go gritha.

All the powders make into fine form by filtering it through a fine cloth of 100

mesh count. “Go gritha” bhavana given to these powders and dried then make into a pill

of 500 mg. This vati/ Gutika were used in the present trial.

Dosage:

Two tablets thrice daily for one week (42 tablets/week) given to patients for every

week until 7 weeks. Blood pressure was recorded for every week. The patients were

advised to take tablets 15-20 minutes after taking food.

If the hypertension severity was less, then used as 1 tablet three times a day.


99

OBSERVATIONS AND RESULTS:

Method of Assessment:

The clinical improvement in the relief of symptoms like Bhrama, Shirovedana,

Nidranasha and the improvement in the blood pressure was assessed. For the practical

purposes, the severity of hypertension is grouped as below.

S.No. Degree of hypertension Systolic blood

pressure

Diastolic blood

pressure.

1. Normal <120 <80

2. High normal 120-139 80-89

3. Stage I 140-159 90-99

4. Stage II >160 >100

For the convenience of the objective parameter result assessment i.e.,

spygomanometer readings. Each and every patient was categorized into normal/high

normal/stage I/stage II, before and after treatment. By using the above categories the

patient improvement was assessed. The assessment was divided into four categories.

They are No response, Mild improvement, Moderate improvement, and Marked

improvement.

Mild improvement was given when the patient stage of hypertension was comes

from i) Stage I to High normal

ii) Stage II to Stage I.

iii)High normal to Normal

Moderate improvement was given when the patient stage of hypertension was

comes from i) Stage I to Normal

ii) Stage II to High Normal.


100

Marked improvement was given when the patient stage of hypertension was

comes from i) Stage II to Normal.

No response when the patient stays in same stage before and after treatment.

In the present study, 38 patients were registered, out of which there were 8

dropouts during various stages of the clinical study. In 30 patients the clinical study was

completed.

OBSERVATIONS:

For the present clinical trial, 38 patients were selected from O.P/I.P.’s

P.G.Department of Kaya Cikitsa, Govt. Ayurvedic Hospital, Hyderabad, for the

evaluation of “Karpasa Beejadi Gritha Gutika”in the management of “Bhrama” w.s.r to

“Hypertension” Among them, there were 8 dropouts during the course with the

remaining 30 patients the clinical study was completed.

Epidemiological data:

Incidences were observed in 30 cases of Hypertension as per schedule described

earlier. The observations are shown in the tables as well as graphs.


101

1. INCIDENCE OF SEX:

Table No. 1 Showing the incidence of sex in 30 patients of Hypertension.

showing the incidence of sex

Male

Female

S.No. Sex No. of patients Percentage

1. Male 15 50%

2. Female 15 50%


102

2. INCIDENCE OF AGE:

Table No.2 Showing the incidence of age in 30 patients of Hypertension.

S.No. Agegroup

No. of Malepatients

No.ofFemalepatients

Percentage

1. 1-25yr 2 0 6.66%

2. 26-35yr 0 2 6.66%

3. 36-45yr 3 2 16.66%

4. 46-55yr 7 4 36.66%

5. 56-65yr 2 5 23.33%

6. 66-75yr 1 2 10

M, 2

F, 0 M, 0

F, 2

M, 3

F, 2

M, 7

F, 4

M, 2

F, 5

M, 1

F, 2

0

1

2

3

4

5

6

7

1-25yr 26-35yr 36-45yr 46-55yr 56-65yr 66-75yr

Showing the incidence of age and sex in 30patients of hypertension

M

F


103

3. INCIDENCE OF RELIGION:

Table No.3 Showing the incidence of Religion

S.No. Religion No. of patients Percentage

1. Hindu 25 83.33%

2. Muslim 5 16.66%

Showing the incidence of Religion

Hindu, 83%

Muslim,17%

HinduMuslim


104

4. INCIDENCE OF MARITAL STATUS:

Table No.4 Showing the incidence of Marital Status in 30patients ofHypertension.

S.No. Marital Status No. of patients Percentage

1. Married 28 93.33%

2. Unmarried 02 6.66%

Showing the incidence of marital status

28; 93%

2; 7%

Married

Unmarried


105

5. INCIDENCE OF OCCUPATION:

Table No.5 Showing the incidence of Occupation in 30 patients of Hypertension.

S.No. Occupation No. of patients Percentage

1. House wife 11 36.66%

2. Doctor 02 6.66%

3. Employ 09 30%

4. Labourer 07 23.33%

5. Students 01 3.33%

Showing the incidence of Occupation

11

2

97

10

2

4

6

8

10

12

Housewife Doctor Employ Labourer Student


106

6. INCIDENCE OF SOCIO-ECONOMIC STATUS:

Table No.6 Showing the pattern of Socio-Economic Status.

S.No. Socio-economic status No. ofpatients

Percentage

1. Low income group 18 60%

2. Middle income group 10 33%

3. High income group 2 7%

Showing the incidence of economical status

LIG, 18, 60%

MIG, 10, 33%

HIG, 2, 7%

LIGMIG

HIG


107

7. INCIDENCE OF FOOD HABITS:

Table No.7 Showing the incidence of Diet

S.No. Diet No. of patients Percentage

1. Vegetarian 4 12.9%

2. Mixed 27 87.1%

Showing the incidence of Diet

Vegetarian, 6,20%

Mixed, 24, 80%

Vegetarian

Mixed


108

8. INCIDENCE OF ADDICTIONS:

Table No.8 Showing the incidence of addictions.

S.No. Addiction No. of patients Percentage

1. Smoking Chewing 01 3.33%

2. Alcohol 03 10%

3. Alcohol+Tobacco smoking 02 6.66%

4 Alcohol+T.Smo+T.Chew 04 13.33%

5 T.Smok+T.Chew. 01 3.33%

6. Toddy+T.Chew. 01 3.33%

7. Alco.+T.Smok+Toddy. 04 13.33%

8. No addictions 12 40%

9. Toddy 05 20%


109

Incidence of addiction in 30 hypertension patients

1

32

4

1 1

4

12

5

0

24

68

1012

14

Smokin

g Che

wing

Alcoh ol

Alcohol+

Tobacco sm

oking

Alcohol

+T.Smo+T

.Chew

T.Sm

ok+T.C

hew.

Toddy+

T.Chew.

Alco.+

T.Sm

ok+Todd

y.

Noa dd

ictions

Toddy


110

9. INCIDENCE OF FAMILY HISTORY:

Table no.9 showing the incidence of Family history of Hypertension.

S.No. Family H/O.Hypetension

No. of patients Percentage

1. Yes 14 46.66%

2. No 16 53.33%

Yes, 14No, 16

02468

10121416

Yes No

Showing the incidence of family H/o Hypertension


111

10. INCIDENCE OF AVAILABILITY OF CASES:

Table No.10 Showing the incidence of availability of cases.

S.No. Availability No. of patients Percentage

1. Fresh 10 40%

2. On medication 20 60%

10

20

0 5 10 15 20

Fresh

OnMedication

Showing the incidense of availability of cases


112

11.INCIDENCE OF HABITATE:

Table No.11 Showing the incidence of Habitate.

S.No. Habitate No. of patients Percentage

1. Town 19 63.33%

2. Rural 9 30%

3. Urban 2 6.66%

Showing the incidence of habitate

19

2

9

02468

101214161820

Town Urban Rural


113

12. INCIDENCE OF SEVERITY BEFORE TREATMENT:

Table No.12 Showing the incidence of Type of Severity of hypertensionBefore treatment.

S.No. Type of Severity No. of patients Percentage

1. High Normal 1 3.33%

2. Stage I 4 13.33%

3. Stage II 25 83.33%

14

25

0

5

10

15

20

25

High normal Stage I Stage II

Showing the severity of hypertension beforetreatment


114

13. INCIDENCE OF OBESITY:

Table No.13 Showing the incidence of Obesity in thirty patients of hypertension.

S.No. Type of Obesity No. ofpatients

Percentage

1. Obese 11 36.66%

2. Non-Obese 19 63.33%

11

19

0 5 10 15 20

Obese

Non-Obese

Showing the indidense of obesity in 30 patients ofhypertension


115

14. INCIDENCE OF CHRONICITY:

Table No.14 Showing the incidence of Chronicity of Hypertension.

Showing the incidence of chronicity ofhypertension

10

6

1

7

4

2

0

2

4

6

8

10

12

Fresh 1mon-6months

6mon-1year 1yr-5yr 5yr-10yr 10yr-15yr

S.No. Chronicity No. of patients Percentage

1. Fresh 10 33.33%

2. 1m-6months 6 20%

3. 6m-1year 1 3.33%

4. 1yr-5yr 7 23.33%

5. 5yr-10yr 4 13.33%

6. 10yr-15yr 2 6.66


116

15.INCIDENCE OF EDUCATION:

Table No.15 Showing the Incidence of Education in 30 patients of Hypertension.

S.No. Education No. of patients Percentage

1. Low Education 13 43.33%

2. High Education 6 20%

3 No Education 11 36.66%

Showing the incidence of Education

13

6

11

0

2

4

6

8

10

12

14

Low education High education No education


117

16.INCIDENCE OF PRAKRITI:

Table No. 16 Showing the pattern of Deha Prakriti in 30 patients of hypertension.

S.No. Deha Prakriti No. of patients Percentage

1. VATAPITTA 12 40%

2. PITTAKAPHA 7 23.33%

3. KAPHAVATA 3 10%

4. PITTAVATA 1 3.33%

5. KAPHAPITTA 4 13.33%

6. VATAKAPHA 3 10%

PK23.33%

KV10%

VP40%

KP13.33% VK

10%PV

3.33%

05

10152025303540

PK KV VP KP VK PV

Showing the incidence of Prakriti in 30 patients


118

17.INCIDENCE OF STRESS:

Table No.17 Showing the incidence of Stress present in 30 hypertensive patients.

S.No. Nature of Stress No. of patients Percentage

1. No stress 4 13.33%

2. Psychological 19 63.33%

3. Psychological+Physical 7 23.33%

413.33%

1963.33%

723.33%

0 10 20 30 40 50 60 70

No stress

Psychologicalstress

Physi+Psycostress

Showing the incidence of type of stress present inpatients


119

18. INCIDENCE OF DIABETES MELLITIS ASSOCIATION:

Table No.18 Showing the presence of Diabetes mellitus.

S.No. Diabetes Mellitis No. of patients Percentage

1. Present 06 20%

2. Absent 24 80%

Showing the incidence of DM along withHypertension

6

24

0

5

10

15

20

25

30

Present Absent


120

19.INCIDENCE OF PATIENTS USINGOTHER MEDICATION:

Table No.19 Showing the Incidence of patients using allopathic drug along with trialdrug in 30 patients of hypertension.

S.No. Type of Drug No. of patients Percentage

1. No drug 09 40%

2. Beta blocker 7 23.33%

3. Betablocker+CCB

5 16.66%

4. CCB 4 13.33%

5. ARB+D 1 3.33%

6. CCB+D 1 3.33%

7. ARB 1 3.33%

8. ACEI 1 3.33%

9. Diretics 1 3.33%

CCB=Calcium channel blocker; ARB=Angiotensin II receptor blocker;D=DireticACEI=Angiotensin converting enzyme Imhibitor.


121

Showing the incidence of using allopathic drug

9

7

4

1

1

5

1

1

1

0 2 4 6 8 10

No drug

BB

CCB

ARB+D

CCB+D

CCB+BB

D

ACEI

ARB


122

RESULTS:

Results were assessed on the basis of clinical (Subjective parameter) as well as

Sphygmomanometer readings (Objective parameter) after the treatment.

RESULTS OF SUBJECTIVE PARAMETERS:

BHRAMA

Table No.20

TotalSymptomGrading

ScoreMean

Meanx-x

S.D. S.E.‘t’

value‘p’

valueRemarks

BT 2.5 1.6 0.50 0.09

AT 0.9 1.6 0.60 0.1117.58 0.000 S


123

SHIRAH SHULA

Table No.21

TotalSymptomGrading

ScoreMean

Meanx-x

S.D. S.E.‘t’

value‘p’

value Remarks

BT 1.96 1.13 0.55 0.10

AT 0.83 1.13 0.53 0.0914.29 0.000 S

ANIDRA

Table No.22

TotalSymptomGrading

ScoreMean

Meanx-x

S.D. S.E.‘t’

value‘p’

value Remarks

BT 0.86 0.50 1.00 0.18

AT 0.36 0.50 0.55 0.104.35 0.000 S

OVER ALL THE SYMPTOMS

Table No.23

TotalSymptomGrading

ScoreMean

Meanx-x

S.D. S.E.‘t’

value‘p’

value Remarks

BT 5.33 3.23 1.24 0.22

AT 2.10 0.50 1.12 0.2019.72 0.000 S


124

Table No.24 Results based on the Subjective parameters.

S.NO. Relief No. of patients Percentage

1. Marked 11 36.66%

2. Moderate 14 46.66%

3. Mild 3 10%

4. No relief 2 6.66%

Showing the results based onsubjective parameters

11, 37%

14, 46%

3, 10%

2, 7%

MarkedModerateMildNo relief


125

RESULTS OF OBJECTIVE PARAMETERS:

Table No.25 Showing the results Based on Systolic blood pressure.

showing the results of SBP beforeand after treatment

0

50

100

150

200

1 4 7 10 13 16 19 22 25 28

BTAT

Objectiveparameter

Mean % ofrelief

Meanof x-x

SD SE ‘t’value

‘p’value

Remarks

BT 158 16.96 3.09S.B.P

AT 131 17.08% 27.33 18.88 3.44 16.50 0.000 S


126

Table No.26 Showing the results Based on Diastolic blood pressure.

Objectiveparameter

Mean % ofrelief

Meanof x-x

SD

SE ‘t’ value ‘p’value

Remarks

BT 103 9.43 1.72D.B.P

AT 90 12.62% 12.83 9.14 1.66 22.45 0.000 S

showing the DBP before and aftertreatment

020406080

100

120140

1 4 7 10 13 16 19 22 25 28

BTAT


127

Table No.27 Results based on Objective parameters.

S.NO. Relief No. ofpatients

Percentage

1. Marked 1 3.33%

2. Moderate 9 10%

3. Mild 14 46.66%

4. No response 6 20%

Showing the results based onobjective parameter.

Marked3%

Moderate30%

Mild47%

Noresponse

20% MarkedModerateMildNo response


128

DISCUSSION:

“Bhrama” is one of the major symptom in hypertension. Along with bhrama other

symptoms like shirah shula and anidra etc., are associated in hypertension.Bhrama occurs

due to vata, pitta prakopa and rajo dosha adikyatha.

Hypertension is one of the many modern disorders of which no direct reference is

available in ayurveda. The symptomatology is available in rakta dushti lakshanas to some

extent, and few other in avritha vayu lakshanas,to some more in rasa dushti lakshanas,but

direct reference as a disease is not yet available.

Certain factors can be credited to cause highblood pressure which is within the

frame work of doshadhatu mala principle. It has been observed in earlier chapters that

prana, vyana, udana, sadhaka pitta,avalambaka kapha,manas,uro hridaya,rasa vaha, rakta

vaha,mutravaha srotas are the factors which play a vital role in the pathogenesis of

hypertension.

Pranavayu has a direct control on hridaya by its dharana capacity. Simultaneously

it controls manas and other higher mental faculties’ because of indriya and chitta dharana.

Indriyas are controlled by manas and manas by prana vayu as stated in hatha yoga

pradeepika. Apart from this, pranavayu has dharana capacity on dhamani as stated in

“Ashtanga sangraha”. Thus prana yauu has a triangular control on: i)Manas, indriyas

ii)Hrudaya and iii)Dhamani. Similarly vyana vayu is the guiding force behind rasa rakta

samvahana, ably assisted indirectly by apana vayu because of identical nature of their

functions. Vyana vayu helps sweda, asruk sravana or expulsion from the body where as

apana vayu helps in the explusion of mutra, mala etc., Ama resulting due to improper

metabolism at dhatwagni level, ama has been stated as a regulatory factor which causes

the accumulation of “Kledamsha” and “Snehamsha”in the dhamanis which causes the

decrease in the lumen of dhamani. This decreases or increases the peripheral resistance,

which in turn increases the load on heart resulting in increased cardiac output.


129

Since the causes for high blood pressure are increased cardiac output and

increased peripheral resistance, the role of prana vayu, vyana vayu and udana vayu is

quite evident.

Pranavayu being connected to the functional aspects in manas, hridaya and

dhamani tries to keep rasa, rakta etc., intact where as vyana vayu tries for sravana of rakta

and sweda by moving away from the body. Similarly apana vayu which is responsible for

the elimination of mootradi, is indirectly helping vayana vayu. That is why it has been

observed that two forces prana vayu on one hand vyana vayu and apana vayu on the other

hand, work in opposite directions. This is also evident from the observation in vijaya

rakshita commentary that prana is “Prakarshena anayati, jeevayati”i,e., that which carries

sensation from the body to the brain and which helps any substance to enter into the

body.

Apana is “Apanayati doorikarothi”i.e., that which carries orders from the brain to

body and which helps the substances expelling them out of the body. Vyana vayu is

clubbed in this functional aspect with apana, because it also expels out sweda and rakta.

Thus it is evident that these two act opposite to prana vayu.

The role of manas, Sadhaka pitta in causing hypertension is not insignificant. It

may be “Malinahara sheeela” or any other factor which will disturb the functional aspect

of “Manas”and “Sadhaka pitta”which is a complex of substances which are invariably

essential in connection with some of the higher mental faculties and emotional states.

These psychogenic factors are correlated with prana vayu which also is related to hridaya

and dhamanies and incidentally hridaya and dhamanies are also related to vyana vayu and

apana vayu. Here vyana vayu helps in rasa samvahanam and apana vayu trying to

eliminate the toxic substances like kledamsha etc.,(causing avarodham)through mootra.

The presence of Kledamsha and Snehamsha is related to ama and avalambaka

kapha, because ama has an invariable relation with kapha for its genesis, as kapha vridhi

disturbs dhatwagni vyapara as well causing ama genesis at dhatwagni level. Avalambaka


130

kapha is present in rasa itself. It is rasa which faces an avarodham for its samvahanam in

dhamanis because of sankocha in turn due to adhesion of kledamsha and snehamsha in

them.

Thus it is a vicious circle between the three vayus as stated earlier, Manas,

Sadhaka pitta, Avalambhaka kapha, and Ama which conjoined together more or less,

result in hypertension.

With these factors in view, the present compound “Karpasa Beejadi Gritha

Gutika” contains Guduchi,Aparajitha,Shatavari,Jatamamsi,Karpasa beejam and Go

gritham, have been considered as an ideal combination for samprapthi vighatana.

Guduchi is tridoshahara, immunomodulator, medhyakara and rasayana drug.

Guduchi is jwaraha which acts as swedajananakari which removes swedavarodham and

eliminated toxic substances by sweda. Guduchi was indicated in hridrogas by vanga sena.

It has deepaniya property which increase Agni helps in amapachanam and eliminates

kledamsha thus relieves srotavarodha and kledatva.

Aparajitha has katu, tikta, kashaya rasas, which acts as pittahara and medhyakara.

It is also indicated in shodha also. It is mentioned in manasika vikaras by Rajamarthanda.

Shatavari has madhura, tikta rasa, Sheeta virya and madhura vipaka.It is vatapitta hara

and rasayana drug. A high dose (60mg/kg) of shatavari produced a fall in blood pressure

and depression of the respiration. Its glycosidal faction produced bradycardia and

reduction in forces of contraction. Jatamamsi has tikta, kashaya, madhura rasas, sheeta

virya and katu vipaka which acts as tridoshahara and it has medhya property. It has a

depressant action on central nervous systerm. Which inturn reduces the blood pressure.

It’s aqueous extract and alkaloid extract also showed hypotensive effects on heart, it’s

root powder shows a sedative action, which in turn reduces the blood pressure.


131

Karpasa beeja has a property of katu rasa,ushna viryu and katuvipaka. It is

vatapitta haram, seeds acts as vrishya. It’s leaf powder mentioned as mutrala (diuretic). It

is indicated in muchra krichchra.

“Go gritha” which has madhura rasa, sheeta virya and madhura vipaka. It acts as

vatapitta hara and medhagnivardhakam. It increases the HDL Cholesterol hence it is a

cardioprotective. Acharya Charaka mentioned “Gritha” preparations in so many places

where the pitta lakshanas are aggravated in his chikitsa stana of charaka samhita.

The compound drug “Karpasa Beejadi Gritha Gutika” having the properties of

madhura, tikta, kashaya rasas, Guru snigdha gunas, Sheeta virya and Madhura vipaka

predominantly. Due to madhura, tikta and kahsaya rasas it acts as a vatapitta shamaka.

Most of the drugs are tridosha hara due to this reason this acts on tridoshas.

In the present clinical trial 10 patients are taken as fresh cases who are suffering

with bhrama and hypertension. 20 patients were already under the treatment of allopathic

prescriptions. But, they are suffering with bhrama associated without control on blood

pressure. All the 30 patients were divided into three categories according to JNC-VII

classification. I) high normal II) Stage I hypertension III) Stage II hypertension. One

patient comes under highnormal, in Stage I 4 patients and in stage II 25 patients.

After the seven weeks of medication, the result was assessed in two ways I) based

on subjective parameters II) based on objective parameter. Based on the objective

parameters the assessment gave results as mild improvement was seen in 14

patients(46.66%),moderate improvement was seen in 9 patients(30%),marked

improvement was seen in 1 patients(3.33%) and no response was seen in 6 patients(20%).

In that mild improvement was seen in 8 males and 6 females, moderate improvement was

seen in 3 males and 6 females, marked improvement was seen in 1 male and no response

was seen in 3 males and 3 females.


132

In mild and marked improvement groups males are more improved, whereas in

moderate improvement group females are more improved. In no response group both

males and females are equally responded.

Out of 30 patients 23 patients are in between the age group of 36-65 yrs. 70 % of

the patients are in Madhya vayah. This indicated the prevalence of the disease is more in

middle aged persons. In this age pitta prabhava is more. Pitta has an ashrayashrayi bhava

relation with rakta, which has a major key role in the genesis of bhrama (hypertension).

Among 30 patients 19 patients (63.33%) are from town area, nine patients (30%)

are from rural area and 2 patients(6.66%) belongs to urban area. Due to small sample size

of clinical research we cannot correlate with this habitat.

83%patients (25) belongs to Hindu religion and 17%(5) patients are belongs to

Muslim religion.

Among 30 patients 18 patients(60%) are belongs to minor income group,10

patients(33%) belongs to middle income group and only 2 patients (6.66%) are belongs to

high income group.

In 30 patients 11 patients (36.66%) belongs to obese category. Whose BMI >25

are categorized as obese patients. 19 patients (63.33%) are belongs to non obese category.

In Non obese patients the improvement is better than obese patients. In mild

improvement of obese group four males and one female was responded. Whereas in

moderate group three female patients were responded well, one male and two female

cases of obese patients were not responded. Non obese patients are responded well than

obese patients. In Non obese category 9 patients are improved mildly, 6 patients are

improved moderately, one patient improved markedly, Obese and nonobese patients are

equally responded in non obese category. 2 obese and 2 non obese patients are not

responded for the treatment except in symptomatic relief in bhrama, shirah shula and

anidra; subjective symptoms are relieved equally in obese and non-bese category.


133

Obesity is a close relation with hypertension. Hypertension is due to increased

cardiac output and increased peripheral resistance. Obesity causes arteriosclerosis which

in turn leads to lumen decrease in arteries and leads to hypertension.

Among 30 patients stress was observed. They categorized into no stress group,

psychological stress only group and physical and psychological stress group.

Improvement observed in these groups most of patients (19) belong to psychological

stress only group. In this group mild improvement was seen in 8 patients, moderate

improvement in 6 patients, marked improvement in 1 patient and no response was seen in

3 patients. In physical and psychological stress only group two persons were not

responded to treatment, five are responded mildly, one patient was responded moderately.

Physical and psychological stress causes anxiety in turn it causes secretion of

catacholamines into circulation which causes the vasoconstriction of blood vessels and

leads to hypertension.

All the thirty patients are divided as “Trial drug group”comprising of nine cases

and “allopathic drug using group”comprising of 21 cases. “In allopathic drug using

group” 7 patients are on betablockers, 5 patients are on calcium channel blocker plus

betablocker, 4 patients are on plain calcium channel blocker and remaining 5 patients are

on different classes of antihypertensive drugs. In ‘trial drug group’46.66 % of the patients

responded as mild improvement, 16.66% patients were responded as moderate

improvement, 3.33%patients were responded as marked improvement. In this group

almost all the fresh patients are responded subjectively and objectively. In “allopathic

drug using group” of 21 cases 33.33% of patients had mildly improved, 13.33% of

patients were moderately improved, 16.66% of patients are not responded even though

they are on continuation of trial drug and allopathic drug.

Among 30 patients of hypertension 10 patients were belongs to fresh category.

Who are diagnosed as hypertensive within one month, in this group 4 patients are mildly

improved,4 patients are moderately improved,1 patient was markedly improved and one


134

patient was not responded to the treatment even though he belongs to fresh group. Six

patients were belongs to the group “1month-6months”, in this group 3 patients were

responded mildly, two patients as moderately and one patient was not responded . One

patient belongs to the group of “6months-1 yr” chronicity was responded moderately.

Seven patients were belongs to the group of “1yr-5yr”chronicity, in this 5 patients

responded as mildly, one patient not responded. Four patients were belongs to the

chronicity group of “5yr-10 yr”, in this group one patient was responded as mildly, two

patients were responded as moderately, and one patient was not responded. In “10 yr-

15yr”group one patient was not responded and one patient was mildly responded.

After seeing all the chronicity groups, it was emphasized that all the chronic

sufferers of the hypertension were not responded well to the treatment. But, subjectively

all of them are relieved in symptoms satisfactorily.

Results according to deha prakriti,out of thirty patients twelve patients belongs to

VP prakriti, All the patients are responded in VP prakriti group. In this group, five

patients are mildly responded, five patients are moderately responded. Two patient were

not responded.

Seven patients belong to PK prakriti.Three patients improved mildly, one

patient was improved as moderately and three patients are not responded. Pittam has a

relation with rakta as ashrashrayi bhava relation. Pitta and Rakta prakopa may leads to

bhrama i.e., hypertension. Increase in sadrava pitta and rakta prakopa increase blood

volume in turn increases in cardiac output leads to hypertension. Increase in sadravapitta

leads to agnimandya then leads to ama formation.Which increases the viscosity of the

blood which increases peripheral resistance further leads to hypertension. This may be

the reason for the patients not responded in PK prakriti group.

Three patients belong to VK prakriti and three for KV prakriti, one patient

belongs to PV prakriti. In KP prakriti group also there is no marked improvement

patients. Only mild improved patients are three and one patient improved as moderately.

In VK prakriti group one patient is markedly improved, one patient was not

responded and one patient was mildly responded. In KV prakriti group on patient was

mildly improved, two patients were markedly improved.


135

All the thirty patients were divided into three groups according to their systolic

and diastolic blood pressures based on JNC-VII classification. These three groups are i)

high normal ii) Stage I hypertension group iii) Stage II hypertension group.

Twenty five patients belong to Stage II hypertension, four patients belong to

Stage I hypertension and one patient belongs to high normal. All the no response cases

are from stage II hypertension group only. The intensity of the disease (hypertension)

may be the cause for the no response in the patients of Stage II hypertension category.

According to Subjective parameter,i.e., relief in bhrama,shirah shula and

anidra,mild improvement was seen in 03 patients,moderate improvement was seen in 14

patients,marked improvement in 11 patients and no response was seen in two patients. In

each and every patient the symptoms were responded satisfactorily with or without

reduction in blood pressure.

Except one patient, she complained abdominal discomfort and bloating after in

taking of the tablets, all the other patients not complained any side effects after in taking

the tablets in course of seven weeks.

After stopping the drug occasionally some patients described giddiness with low

intensity when compare with the earlier bhrama.

LIMITATIONS OF THE STUDY:

The sampling method was incidental and sample size was very small, so it is

difficult to generalize the results.

Fluctuations of blood pressure when risk factors are consumed.

RECOMMENDATIONS FOR FUTURE STUDY:

The same study can be conducted with large sample size.

A comparative study of the Ayurvedic and allopathic drugs can be conducted.

An effort should me made to understand our drugs in terms of ACE

inhibitors,Calcium channel blocker,α-blocker,β-blocker,diuretics etc.,

A study can be conducted with other therapies like shirodhara, basthi,

rakamokshana.


136

CONCLUSION:In the present clinical trial “The effect of Karpasa Beejadi Gritha Gutika in tha

management of Bhrama w.s.r.to Hypertention”. 30 cases were studied , out of them 25

cases were having Stage II hypertension, four cases were having Stage I hypertension and

one case has Highnormal. Thus according to the severity of disease the patients were

divided into three groups.

Response to the treatment was classified as no response, mild improvement,

moderate improvement and marked improvement. According to Objective parameter i.e.,

blood pressure reading, In 25 cases of Stage II hypertension 1 case was responded

markedly, 7 cases are moderately, 11 cases are having mild improvement and six cases

were not responded in this group.

In four cases of Stage I hypertension two cases are showed as moderate

improvement and two cases are showed mild improvement.One case of high normal

responded as mild improvement.

According to Subjective parameter,i.e., relief in bhrama,shirah shula and

anidra,mild improvement was seen in 03 patients,moderate improvement was seen in 14

patients,marked improvement in 11 patients and no response was seen in two patients.

Signs and symptoms recorded before and after treatment the commencement of

the treatment have been reviewed finally at the end of the course. Symptoms like knee

joint pains, bronchial asthama and slurred speech associated with hemiplegia are not

responded within the 7 weeks of treatment. But, these conditions are improved when

compare with the schedule initiation.

In ‘Stage II degree of hypertension’ cases were responded well after two weeks of

treatment. In this group almost all the patients more or less responded well. But,

symptomatic relief was achieved within one week of treatment.i.e., relief in


137

bhrama,shirashula and anidra. In this group eleven patients were showed mild

improvement.

All the chronic patients more than five years of history were not responded well.

It may be due to chronicity of the disease. But, symptomatically they are also responded

well.

Thus to sum up the compound drug “Karpasa Beejadi Gritha Gutika” consisting

Guduchi,Aparajitha,Shatavari,Jatamamsi,Karpasa beejam and Go gritham, is useful in

cases of hypertension associated with giddiness(Bhrama). Symptomatically very effective

relief was achieved in Bhrama, Shirashula and Anidra.


138

SUMMARY:The present clinical study conducted from the evaluation of the effect of “Karpasa

Beejadi Gritha Gutika” in the management of “Bhrama” w.s.r to Hypertension.

The word Hypertension explained in introduction. The history of hypertension

from ancient to present period, various references of bhrama and reasons for the disease

why it was not there in those days.

The explanation of definition of Hypertension; Shareera (Anatomy and

Physiology) and Nidana (Pathology) of Hypertension explained, according to ayurveda

and modern literature.

Consequences and pathogenesis of hypertension explained in disease aspect.

Management of Hypertension by modifying, the mental activity and the treatment

of Bhrama (Hypertension) are explained. Dietary restrictions as Pathya-Apathya are

explained.

The criteria for the selection of the drugs and botanical names, disriptions,

indications and uses of the drugs are explained in drug aspect.Importance of go gritha and

its utility in hypertension was explained.

The Number and nature of the cases teken-up for the clinical study has been

stated. Observation before, during and after treatment with results are recorded and

explained.

The results are divided into four categories they are mild improvement, moderate

improvement, marked improvement and no response.

The approach of disease Hypertension discussed. Hatayoaga and Bruhatriyi view

discussed. The effect of compound drug on Hypertension is discussed.

Total study of the disease, drug, and preliminary clinical work has been reviewed,

in a brief discussion. Results of the treatment showing the efficacy of the drug have been

stated effect of the treatment results on both sexes and different age groups Hypertensive

patients have been concluded. The utility of the study is out lined.


139

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DR.B.R.K.R.GOVT.AYURVEDIC COLLEGE.S.R.NAGAR, HYDERABAD-500038.

POST GRADUATDE DEPARTMENT OF KAYACHIKITSA.

SPECIAL CASE SHEET FOR EVALUATION OF “KARPASABEEJADIGRITHA GUTIKA” IN THE MANAGEMENT OF ‘BHRAMA’ WITHSPECIALREFERENCE TO “HYPERTENSION”.

S.No :Name : Case : OP/IPW/o d/o s/o: O.P.Regd.No :Age : D.O.A :Sex : D.O.D :Occupation:Address :Income :1 Chief complaint with duration:

2) Associated symptoms:

3) History of Present illness:

4) History of Past illness:

5) Treatment history:

6) Family history: 1.Mother:2. Father:3. Married/Unmarried4. Children:5. Any other congenital disorders:

7) Personal History:Haibits :Addictions :

Alcohol/Tobaccosmoking/Chewing/Toddy/Cannabis/Noaddiction.Diet : Mixed/Veg.Socioeconomic status:LIG/MIG/HIG

8) Presence of risk factors: i) Smokingii) Diabetesiii) Physical inactivityiv) BMI/BWIv) Alcohol


147

9) Psychological factors:i) Stress-Physicalii) Stress-Psychologicaliii) Type of Job : Private/ Govt./ Individual/ Un employiv) Education : Low education/ High education/ No education

10) Physical examination:

a) Inspection:

b) Palpation:

c) Percussion:

d) Auscultation:

e) General Examination:BP :PR :RR :TEMP :WEIGHT :LIVER :SPLEEN :HEART :LUNG :

f)Dasha vidha Pariksha:PRAKRITHI SAMHANANAVIKRITHI AHARASHAKTHISAARA VYAYAMASHAKTHISATMYAM VAYAHSATVAM PRAMANAM

g)Ashatastana Pariksha:NADI SHABDHAMALA SPARSHAMUTRA DRIKJIHWA AKRITHI

h)Srotopariksha:RASAVAHA SHUKRAVAHARAKTAVAHA PRANAVAHAMAMSAVAHA UDAKAVAHAMEDHOVAHA ANNAVAHAASTHIVAHA SWEDAVAHAMAJJAVAHA ARTAVAVAHA


148

FOLLOWUP:INVESTIGATIONS 1ST

DAY7TH

DAY14TH

DAY21ST

DAY28TH

DAY35TH

DAY42ND

DAY49TH

DAYBP

CBPCUEBODY WEIGHTLIPID PROFILEESRB.UREAS.CREATININEB.SUGARECGBMIBWILFTBS/BP

Conclusion :

Result :

Signature of the Guide

Signature of the Co-Guide.

INFORMED CONSENT

I______________________________son/daughter/wife of____________________________am exercising my free will to participate in abovestudy as a subject. I have been informed to my satisfaction, by attending physician thepurpose of clinical evaluation and the nature of the drug treatment. I also aware of myright to opt out of the treatment schedule, at any time during the course of the treatment.

Patient signature.

Schedule Initiation:

Result: Responded/Not responded/Discontinued.

Siganature of the Co-guide. Signature of the Guide.


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