Effect Of Kbgg In The Management Of Bhrama(hypertension)

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

Dissertation submitted in partial fulfillment for the degree of DOCTOR OF MEDICINE (AYURVEDA) In

“KAYACHIKITSA” By Dr.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, VIJAYAWADA Dr.B.R.K.R. GOVT.AYURVEDIC COLLEGE, HYDERABAD. 2008

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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: Place: Hyderabad.

Dr. V. VIJAYA BABU MD (Ayu) Reader Post graduate Department of Kayachikitsa, Dr. B.R.K.R. Govt. Ayurvedic College, Hyderabad.

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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: Place: Hyderabad

Dr.PRAKASH CHANDER MD (Ayu) Professor& HOD, Post graduate Dept. of Kayachikitsa Dr. B.R.K.R. Govt. Ayurvedic College, Hyderabad.

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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 coguide 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 cooperation.

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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

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LIST OF TABLES: S.No. 1. 2. 3. 4. 5. 6. 7. 8. 9. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35.

Title of the table Table showing the external features of the heart Diagram showing difference between artery and vein. Illustration showing the blood pressure regulation. Illustration showing the ‘rennin-angiotensin system’. Showing the phases of ‘korotkoff sounds’ Schematic representation of ‘samprapthi of bhrama’ with special references to hypertension. Table showing the hypothetical scheme for the pathogenesis of essential hypertension. Table showing initiation of modern treatment in patients with hypertension. Table showing classification and management for Adults Table showing picture of individual drugs Incidence of sex Incidence of age Incidence of religion Incidence of marital status Incidence of occupation Incidence of socioeconomic status Incidence of food habits Incidence of addictions Incidence of family history Incidence of availability Incidence of habitate Incidence of severity before treatment Incidence of obesity Incidence of chronicity Incidence of prakriti Incidence of stress Incidence of diabetes mellitus association Incidence of using other drug Table showing the subjective parameter bhrama Table showing the subjective parameter Shirahshula Table showing the subjective parameter Anidra Table showing the subjective parameter Over all symptoms Table showing results based on subjective parameter Table showing results based on systolic blood pressure Table showing results based on diastolic blood pressure Table showing results based on objective parameter.

Page No. 11 16 20 23 28 56 65 78 80 92 101 102 103 104 105 106 107 108 110 111 112 113 114 115 116 117 118 120 122 123 123 123 124 125 126 127

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INDEX Page no.  Introduction

1.

 Historical Aspect

3.

PART-A:

PART-B:

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

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

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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

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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.

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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 20mmofHg 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,

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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

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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.

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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.

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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 16 th 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.

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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. th

In this adhunika kala our 20 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.

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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 stanas 1. 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 6

para and apara ojus . Hridaya is the prabhava sthana of dashadamanis which spreads all 7

over the body and which carries rasa, ojus and does tarpana karma . 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.

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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

11

bala(strength) , 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 shiras 12, and 13

according to Sharangadhara it is situated in hridaya .Vagbhata states that pranavata maintains the activities of hridaya (heart and circulatory system) and supports or does 14

dharana of dhamanis(probably the vasomotor functions) .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 15

16

Vyana vata is situated in hridaya , and it pervades swiftly throughout the body . 17

Vyana vayu is responsible for circulation of Rasa (rasadhatu) through out the body ,by 18

the regular contraction and relaxation of the heart . 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

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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 22

Sadhaka pitta is situated in hridaya , 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 manas 23. 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 25

srotas . 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 uras 26.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

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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 rd

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

2/3 to 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

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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

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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 24. Cha.sam.Sutra-30/13 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

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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

“Dhmand dhamanyah2”

“Sravanath srotamsi 3”

 Definition: “Saranaat sirah1”  Chakrapani,gangadh

 Chakrapani,gangadh

 Chakrapani,gangadh

ara,gananathsen’s

ara,gananathsen’s

ara,gananathsen’s

Opinion gives in favour of Opinion gives in favour of Opinion gives in favour of vein.

artery.

 Asudda raktavahinis are sira

considered and

as

canbe

referred

as

vein(atharvaveda)  Pittavaha siras canbe considered as vein4  The word sira has

capillaries.

 Shudda raktavahinis are

 It has paryayas like

considered as

sira,dhamani,rasaya

dhamani and canbe

na,nadi,pantha,marg

referred

a etc.,

as

artery(atharvaveda)  The word dhamani has been used with the

meaning

of

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15 been used with the meaning

of

5

kandara .

jnyanatantuvu8.  At

parishad

shabdartha it was

 The word sira has

concluded

that

been used with the

dhamani

meaning

considered as artery,

of

dhamani6.  The

canbe

nerve or vein or any

word

sira

denotes vein, artery 7

and lymphatics .

vessel in the body.  The word dhamani has been used with the

meaning

of

9

rasavahini .  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.

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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.

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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 3

carried out continuously throughout the life .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.

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18 Regarding rasa samvahana acarya sushritha gives a simily i.e.,”Shabdharchi jalasantanavat 4”.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

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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.

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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 factors Constrictors Dilators. -Angiotensin II -Prostaglandins -Catacholamines -Kinins * -Thromboxane -NO/EDRF -Leukotriens -Endothelin

Blood volume -Sodium -Mineralo corticoids -Atriopeptine

BP=Cardiac Out put X Peripheral Resistance

Cardiac factors -Heart rate -Contractility

Neural factors Constrictors Dilators -αadrenergic -βadrebergic

Local factors -Autoregulation. -Ion(HP,Hypoxia)

*Endothelin derived relaxing factor.

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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

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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.

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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

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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.

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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.

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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.

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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.

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28

Showing the phases of korotkoff sounds:

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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.

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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

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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

i)parenchyma

2-3

4-5

ii)Reno vascular

1-2

4-16

i)Primary aldosteronism

0.3

0.5-12

ii)Pheochromocytoma

<0.1

0.2

pill 0.5-1

1-2

B.Renal hypertension

C.Endocrinal hypertension

iii)Oralcontraceptive induced hypertension D.Miscellaneous

0.2

1

Some of the other forms of hypertension are :

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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.

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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 2

disease. Which is manifested due to prakopa of vata,pitta and rajo guna . 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 4

on the ground . 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 prakopa 5 . 2. Anashana, Adyashana, Vishamashana, Vishamopacharam, Viruddahara sevana can also cause vata prakopa6. 3.Sushkashaka,Vallura,Varakoddalaka,,Koradoosha,Shyamaka.Neevara,Mudgara, 7

Masura,Adhaki,Harenu,Kalaya Nishpava .

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34

b) Viharaja: 1.

Ativyayama,

Vegasandharana,

Vyavaya,

Jagarana,

Bharaharana,

Gajaturagaradha padhaticharya 8, Prapatana, Bhagnam.

c) Panchkarmajanya: 1. Vamana, Virechana, Shirovirechana atiyogas 9 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 aggravation 13. 3. Tila, Atasi, Dadhi, Sura, Sukta, Aranaala and Kuluttha. 4. Dushtannam 5. Vidahi padartha sevana 14

6. Ahara vidahikala 7. Ksharam15.

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35 b) Viharaja: 1. Teekshan atapa sevana, Agni santapa can cause pitta prakopa. 2. Shrama, Krodham16.

c) Pancha karmajanya: 17

1. Vamana, Virechana and Nasyakarma atiyogam . 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.

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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.

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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 generations 1.

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 3

veerya of the parents at the time of conception .

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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 4

and leads to shonitaja roga . 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.

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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. 7

Sushrutha has mentioned medoroga leads to vata vikara . 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 pratichaya 8 (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 nerveendings 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

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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 9

hypertension .

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 10

caused by them are kama, krodha, lobha, moha, bhaya etc ., Acharya charaka has advised to suppress these factors 11,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 14

15

oja which is also ashrita of hridaya , and vitiation of vata and pitta , 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.

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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 include1) 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.

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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 socioeconomic 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.

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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 agerelated 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

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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 hypertension 20.

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45

References: 1. Cha.sam.sha-3/17 2. Sushritha sam. Shar-4/36 3. Sushritha sam. Sutra-24/5 4. Cha.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

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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 rupavasta 2,3. 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.

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RUPAM: The collection of symptoms which can indicate the present disease is known as 1

rupam . The symptoms of established disease are known as Rupas2. The synonyms for the Rupam 3 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 jwara 7.

In other chapters the rupam bhrama mentioned as

Disease

Author 8

1.Pittaja kasa

Astanga hridaya nidana

2.Pittaja hridroga

9

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 chardi

15

Madava nidana

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48 8.Vataja arshas 16,17

Asta.Hri.Nidana/Madava nidana

9.Vata kundalika18

Asta.Hri.Nidana

10.Vata vidradi

19

Asta.Hri.Nidana

11.Pittaja udaram/Sannipata udara 20,21

Asta.Hri.Nidana/Madava nidana

12.Pandu 22

Asta.Hri.Nidana 23

13.Halimakam

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 Astanga hri.nidana/Sus.sam. nidana

medogata/Pittavrita vata/Pittavrita prana vata/Pittavrita udana vata/PK yukta udana vata 28 18.Krimi29

Madavanidana 30

19.Marma kshata

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

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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.nidana19. 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

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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 factors 3. 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 vata 4.

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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 prakopa 6. In sharath ritu pitta prakopa occurs and when teekshnadi pitta gunas associated 7

with ushna guna leads to pitta prakopa .

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 8

place for the disease .

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.

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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 forcing him 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 12

establishes as a disease. But, it is not possible to name every disease .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 Madhavakara 18. When bhrama occurs in madatyaya rogi it becomes asadhyam19.

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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

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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

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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-

Manasika-

vata-

vyana, prana, udana

Pitta-

pachaka, sadhaka

Kapha -

avalambaka.

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.

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56

SCHEMATIC REPRESENTATION OF SAMPRAPTHI OF BHRAMA 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

Narrowing of blood vessels.

Medho Dushti.

Vata

Pitta

Rakta

Increased heart Rate.

Kapha

Viscosity of blood. Cardiac Output Bhrama

Blood volume Peripheral resistance Hypertension

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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.

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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.

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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

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60 -Occlusion and stenosis -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.

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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 controlling1. 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 extracellular sodium ion concentration, thus leading to a disturbance of sodium homeostasis.

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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.

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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-angiotensinaldosterone 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.

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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.

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65

Table showing the hypothetical scheme for the pathogenesis of Essential hypertension:

Genetic influences

Environmental factors

Defects in renal sodium hemostasis

Inadequate sodium excretion

Salt and Water retention

Plasma & ECF volume

Vascular reactivity

Cardiac Output

Vascular wall thickness

Total peripheral resistance Hypertension

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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

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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.

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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.

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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 Often develops before the age

hypertension, along with reported of 35or after 55.history of use finding

of

intermittent

pressure of steroids or estrogens is of

elevation in the past favours the obvious significance. diagnosis of essential hypertension. PATHOLOGY

Pathogenesis

is

not

clearly Pathogenesis and pathology

understood and pathology pertains to depends on the disease that has heart and blood vessels

caused hypertension.

BLOOD

A rise in diastolic pressure when the A fall in the absence of

PRESSURE

patient goes from the supine to the antihypertensive

RECORDING

standing position is most compatible with the treatment of the cause, with essential hypertension.

medication

suggest secondary forms of hypertension.

SYMPTOMS

Symptomatic

or

asymptomatic, Symptoms will be present with

vague symptoms like headache, the underlying disease. bhrama, easy fatigability etc., will be present. INVESTIGATI Urine ONS

analysis

and Depending on underlying the

microscopy,serumurea,creatinine,uri

disease, the values of these

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70 cacid,serum

electrolytes,fasting laboratory investigations and

glucose,fasting lipids,ECG and chest ECG and chest X-ray varies. X ray. The values of all laboratory Here some special studies are investigations will be within normal needed to screen for secondary range. ECG and chest X-ray will be hypertension. normal. PROGNOSIS

It

is

controllable

with

proper It is curable .when cause is

treatment. It requires life long treated, the elevated blood monitoring

TREATMENT

and

treatment

may pressure

comes

require periodic adjustments.

normal.

Treatment comprises of

Treatment

1.Non drug therapy

cause

and

 Relief of stress

therapy

 Dietary management

condition.

down

depends

on

requires during

to

the drug

severe

 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

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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.

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72

COMPLICATIONS OF ESSENTIAL HYPERTENSION: ORGAN

BRAIN

COMPLICATIONS ATHEROSCLEROTIC

PRESSURE INDUCED

Cerebralinfarction,

Hypertensiveencephalopathy,

Transient

EYE

ischaemic Cerebral haemorrhage,

attacks

Lacunar infarcts

Retinal vascular accidents

Exudative

and

haemorrhagic

changes,Papilloedema. HEART

Angina,Myocardiac

Hypertensive

heart

disease,

Left

infarction,Sudden death

ventricularhypertrophy,cardiomagaly, ECGabnormalities, congestive cardiac failure.

KIDNEY

Renovascular disease

Arteriolar nephrosclerosis, Benign-without fibrinoid, Malignant-with fibrinoid.

PERIPHERAL

Intermittentclaudication,

ARTERIES

Vascular occlusion.

Aneurysms, aortic dissection.

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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:

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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.

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CHIKITSA: 1

Vyadhiharana kriyas are known as chikitsa . Roga nidana pratikaras are also 2

3

called as chikitsa . Sushritha mentioned as “nidana parivarjana” as a chikitsa .

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 5

6

“pittavrita prana vata” by charaka and vagbhata .Charaka mentioned treatment for “pittavrita vata” in his chikitsa stana 7.

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 8

and ksheera vastis are also mentioned .

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.

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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.

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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

Sodium restriction

Dietary

Relaxation

advice

B.P.REDCUTION(mmofHg.) sodium 8-15 systolic

intake(<100m mols/day)

5-6 diastolic

Relaxation techniques

9-27 systolic 4-16 diastolic

Weight loss

Diet and exercise

Exercise

Aerobic programme

9-27 mean arterial pressure exercise 6-13systolic 9-12 diastolic.

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78

Table showing initiation of modern treatment in patients with hypertension.

SBP 140-180 (or)

DBP 90-110 mmofHg.

Assess other risk factors

TOD

Initiate life style mesures

Stratify absolute risk

Veryhigh

Begin with Drug

SBP≥140 or DBP≥90 Begin Drug.

High

Begin with Drug

SBP ≤140 or DBP ≤90 Continue to Monitor

Medium

Low

Monitor BP& Other risk factors for 36months

Monitor BP & Other risk factors for 6-12 months

SBP ≥150 orDBP ≥95 Begin Drug.

SBP ≤150 DBP ≤95 Continue to Monitor

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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

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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.

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81

CLASS

COMPELLING

POSSIBLE

COMPELLING

POSSIBLE

OF

INDICATIONS

INDICATIONS

CONTRA

CONTRA

INDICATIONS

INDICATIONS

Gout

Dyslipidemia,

DRUG DIURE

Heart

TICS

elderly

failure, Diabetes patients,

sexually

systolic

active

males

hypertension. Β-

Angina,

BLOCKE

myocardial

pregnancy,

infarct,

diabetes

RS

after Heart

failure, Asthma, COPD, Dyslipidemia, heart block.

athletes &physically active

tachyarrhythmias

patients, peripheral vascular disease

ACE INHI

Heart

failure,

BITORS

LVF,

after

Pregnancy, hyperkalaemabi

myocardial

lateral

infarct,

artery stenosis.

diabetic

renal

nephropathy. CALCIM

Angina,

ANTA

patients, systolic vascular disease

GONISTS

elderly Peripheral

Heart block

Congestive

heart

failure

hypertension

Α-BLOCK

Prostatic

Glucose

Orthostatic

ERS

hypertrophy

intolerance,

hypotension.

dyslipidemia ANGIOTE

ACE-inhibitor

NSIN

cough.

II

ANTAGO NISTS

Heart failure

Pregnancy,hype rkalaemia, bilateral

renal

artery stenosis.

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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):

AHARA

PATHYA

APATHYA

Mudga,masoora,yava,palaka,

Anupa desha pakshimamsa,

methica,jambeera,carrot,papaya,

dadhi,dugda vikara,tobacco,tea,

drygrapes,orange,ardraka,rasona,

coffee,salt,fatty substances,

hingu,jeeraka,maricha,

alcohol,etc.,

jangala pakshi mamsa,godugda, ajadugdha,takra etc., VIHARA

Samyakvishrama,upavasa,shavasaa,

Diasvapna,ativyayama,avyayama,

samyak vyayama,sadvrittapalana,

vegadharana,adhyashana,

nitya abhyanga,Krodha-irsha-bhaya- atichintana,atikrodha,atishrama, chinta-shokadi

dharaniya

vega atisukhasana,ratrijagarana etc.,

dharana,etc.,

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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.

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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 1

from roots.It is mentioned in Hridroga by vanga sena .

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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.

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.

Properties:

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.

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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.

Chemical constituents: From roots:

Sarasapogenin,two

spirostanolic

and

two

furostanolic

sponins,sitosterol,asparaganine A.

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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: 1. Bhava prakasha nighantu. “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.

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.

Properties:

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88

Chemical constituents: 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.

RASA

:

Katu

GUNA

:

Tikshna, Snigdha (Root bark-Laghu)

VIRYA

:

ushna

VIPAKA

:

Katu

Properties:

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89 KARMA

:

VP hara, Seed-vrishya, Leaf-mutrala, stanya janana.

INDICATIONS

:

PARTS USED

:

Root, Flower, Seed.

DOSE

:

Decoction: 50-100ml;

Karna puya, karnanada, mutrakrichcha, anartava, kashtartava.

Seed powder: 3-6 gm.

Chemical constituents: Root

:

hemigosypol;

Flowers

:

quercimetitrin;

Seed

:

gossypol;

Essential oil

:

caryophyllene, Pinene, Limonene.

References: 1. Bhava prakasha nighantu. “Karpasako …….tatbheejam syandham vrishyam snigdham kaphakaram guru” 1

Toxic effects of G.Herbacium : 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 2

preventing the onset of symptoms .

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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

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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)

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92

PICTURES OF INDIVIDUAL DRUGS:

GUDUCHI

APARAJITHA

SHATAVARI

JATAMAMSI

KARPASA

GO GRITHAM

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93

KARPASA BEEJAM

KARPASA BEEJAM SECTION CUTTING

“KARPAASA BEEJADI GRITHA GUTIKA”:

KARPASABEEJADI GRITHA GUTIKA

KARPASABEEJADI GRITHA GUTIKA

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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.

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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.

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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.

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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 -Occlusion and stenosis -Cardio Vascular diseases -Cardio vascular diseases. -Sequel of Cardio vascular diseases.  Involving vessels of Eye and Retinal disorders.

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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.

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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

Diastolic blood

pressure

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.

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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.

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1. INCIDENCE OF SEX: Table No. 1 Showing the incidence of sex in 30 patients of Hypertension.

S.No.

Sex

No. of patients

Percentage

1.

Male

15

50%

2.

Female

15

50%

showing the incidence of sex

Male Female

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102

2. INCIDENCE OF AGE: Table No.2 Showing the incidence of age in 30 patients of Hypertension.

S.No.

Age group

No. of Male patients

No.of Female patients

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

Showing the incidence of age and sex in 30 patients of hypertension M, 7

7 6

F, 5

5 F, 4

4

2

M

M, 3

3 M, 2

F, 2

F, 2

M, 2

F

M, 1

1 0

F, 2

F, 0 1-25yr

M, 0 26-35yr

36-45yr

46-55yr

56-65yr

66-75yr

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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

Muslim,17% Hindu, 83%

Hindu Muslim

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104

4. INCIDENCE OF MARITAL STATUS: Table No.4 Showing the incidence of Marital Status in 30patients of Hypertension.

S.No.

Marital Status

No. of patients

Percentage

1.

Married

28

93.33%

2.

Unmarried

02

6.66%

Showing the incidence of marital status

2; 7%

Married Unmarried

28; 93%

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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 12 10 8 6

11 9

4

7

2 2

1

0 Housewife

Doctor

Employ

Labourer

Student

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106

6. INCIDENCE OF SOCIO-ECONOMIC STATUS: Table No.6 Showing the pattern of Socio-Economic Status. S.No.

Socio-economic status

No. of patients

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

HIG, 2, 7%

LIG MIG

MIG, 10, 33% LIG, 18, 60%

HIG

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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% Vegetarian Mixed Mixed, 24, 80%

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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%

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109

Incidence of addiction in 30 hypertension patients 14

12

12 10 8 6

4

3

4 2

2

1

5

4 1

1

0

Sm

g in ok

C

w he

g in

A

o oh c l

l ho o c Al b To + l

co ac

sm

o lc A

i ok

ng

m S T. + l ho

.

.

y. ns io dd t o c C .C T di T. +T + k+ ad y o k o m dd No .S Sm To . T T + o. lc A

C T. + o

he

w

w he

he

w

dd To

y

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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%

Showing the incidence of family H/o Hypertension

16 14 12 10 8 6 4 2 0

Yes, 14

Yes

No, 16

No

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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%

Showing the incidense of availability of cases

20 On Medication

10 Fresh

0

5

10

15

20

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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 20 18 16 14 12 10 8 6 4 2 0

19

9

2 Town

Urban

Rural

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113

12. INCIDENCE OF SEVERITY BEFORE TREATMENT: Table No.12 Showing the incidence of Type of Severity of hypertension Before 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%

Showing the severity of hypertension before treatment 25 25 20 15 10 5

4 1

0 High normal

Stage I

Stage II

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114

13. INCIDENCE OF OBESITY: Table No.13

Showing the incidence of Obesity in thirty patients of hypertension.

S.No.

Type of Obesity

No. of patients

Percentage

1.

Obese

11

36.66%

2.

Non-Obese

19

63.33%

Showing the indidense of obesity in 30 patients of hypertension

19

Non-Obese

11

Obese

0

5

10

15

20

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115

14. INCIDENCE OF CHRONICITY: Table No.14 Showing the incidence of Chronicity of Hypertension. 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

Showing the incidence of chronicity of hypertension 12

10

10 7

8

6

6

4

4

2 1

2 0 Fresh

1mon6months

6mon-1year

1yr-5yr

5yr-10yr

10yr-15yr

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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 14

13 11

12 10 8

6

6 4 2 0 Low education

High education

No education

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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%

Showing the incidence of Prakriti in 30 patients VP 40% 40 35 30 25 20 15 10 5 0

PK 23.33% KP 13.33%

KV 10%

PK

KV

VP

KP

VK 10%

VK

PV 3.33% PV

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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%

Showing the incidence of type of stress present in patients

7 23.33%

Physi+Psyco stress

19 63.33%

Psychological stress 4 13.33%

No stress 0

10

20

30

40

50

60

70

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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 with Hypertension 30 24

25 20 15 10

6

5 0 Present

Absent

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120

19.INCIDENCE OF PATIENTS USING OTHER MEDICATION: Table No.19 Showing the Incidence of patients using allopathic drug along with trial drug 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.

Beta blocker+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=Diretic ACEI=Angiotensin converting enzyme Imhibitor.

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121

Showing the incidence of using allopathic drug ARB

1

ACEI

1

D

1

CCB+BB

5

CCB+D

1

ARB+D

1

CCB

4

BB

7

No drug

9 0

2

4

6

8

10

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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 Total Symptom Grading Score Mean

Mean x-x

S.D. 

S.E.

BT

2.5

1.6

0.50

0.09

AT

0.9

1.6

0.60

0.11

‘t’ value

‘p’ value

Remarks

17.58

0.000

S

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123 SHIRAH SHULA Table No.21 Total Symptom Grading Mean Score x-x Mean BT AT

1.96 0.83

1.13 1.13

S.D. 

S.E.

0.55

0.10

0.53

‘t’ value

‘p’ value

Remarks

14.29

0.000

S

‘t’ value

‘p’ value

Remarks

4.35

0.000

S

‘t’ value

‘p’ value

Remarks

19.72

0.000

S

0.09

ANIDRA Table No.22 Total Symptom Grading Mean Score x-x Mean BT AT

0.86 0.36

0.50 0.50

S.D. 

S.E.

1.00

0.18

0.55

0.10

OVER ALL THE SYMPTOMS Table No.23 Total Symptom Grading Mean Score x-x Mean BT AT

5.33 2.10

3.23 0.50

S.D. 

S.E.

1.24

0.22

1.12

0.20

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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 on subjective parameters 2, 7% 3, 10%

14, 46%

11, 37%

Marked Moderate Mild No relief

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125

RESULTS OF OBJECTIVE PARAMETERS:

Table No.25 Showing the results Based on Systolic blood pressure.

Objective Mean parameter S.B.P

% of Mean SD  relief of x-x

SE

‘t’ value

BT 158

16.96

3.09

AT 131 17.08% 27.33

18.88

3.44 16.50

‘p’ Remarks value

0.000

S

showing the results of SBP before and after treatment 200 150 BT AT

100 50 0 1

4

7

10 13

16 19 22 25 28

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126 Table No.26 Showing the results Based on Diastolic blood pressure.

Objective Mean parameter

% of Mean relief of x-x

BT

103

AT

90

D.B.P

12.62%

12.83

SD 

SE

9.43

1.72

9.14

1.66

‘t’ value ‘p’ value

22.45

0.000

Remarks

S

showing the DBP before and after treatment 140 120 100 80 60 40 20 0

BT AT

1

4

7

10 13 16 19 22

25 28

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127 Table No.27 Results based on Objective parameters.

S.NO.

Relief

No. of patients

Percentage

1.

Marked

1

3.33%

2.

Moderate

9

10%

3.

Mild

14

46.66%

4.

No response

6

20%

Showing the results based on objective parameter. No response 20%

Marked 3% Moderate 30%

Mild 47%

Marked Moderate Mild No response

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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.

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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

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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.

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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.

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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.

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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

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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 yr15yr”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.

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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.

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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

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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.

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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.

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139

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145 84. Subrahmanya Sastry.V.V.; Essentials of Basic Ayurvedic Concepts; Publication Division, P.G. & Research Center, Sri. D.G.Malmalagi Ayurvedic Medical College, Gadag (1999). 85. Nadkarni.K.M, Indian Materia medica, Popular Prakashan Pvt. Ltd., Bombay, Second reprint of 3rd revised Edn, 1982.

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146 DR.B.R.K.R.GOVT.AYURVEDIC COLLEGE. S.R.NAGAR, HYDERABAD-500038. POST GRADUATDE DEPARTMENT OF KAYACHIKITSA. SPECIAL CASE SHEET FOR EVALUATION OF “KARPASABEEJADI GRITHA GUTIKA” IN THE MANAGEMENT OF ‘BHRAMA’ WITH SPECIALREFERENCE TO “HYPERTENSION”. S.No : Name : W/o d/o s/o: Age : Sex : Occupation: Address : Income : 1 Chief complaint with duration:

Case O.P.Regd.No D.O.A D.O.D

: OP/IP : : :

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/Unmarried 4. 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) Smoking ii) Diabetes iii) Physical inactivity iv) BMI/BWI v) Alcohol

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147 9) Psychological factors: i) Stress-Physical ii) Stress-Psychological iii) Type of Job : Private/ Govt./ Individual/ Un employ iv) 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 VIKRITHI SAARA SATMYAM SATVAM

: : : : : : : : : SAMHANANA AHARASHAKTHI VYAYAMASHAKTHI VAYAH PRAMANAM

g)Ashatastana Pariksha: NADI MALA MUTRA JIHWA

SHABDHA SPARSHA DRIK AKRITHI

h)Srotopariksha: RASAVAHA RAKTAVAHA MAMSAVAHA MEDHOVAHA ASTHIVAHA MAJJAVAHA

SHUKRAVAHA PRANAVAHA UDAKAVAHA ANNAVAHA SWEDAVAHA ARTAVAVAHA

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148 FOLLOWUP: INVESTIGATIONS 1ST DAY BP

7TH DAY

14TH DAY

21ST DAY

28TH DAY

35TH DAY

42ND DAY

49 TH DAY

CBP CUE BODY WEIGHT LIPID PROFILE ESR B.UREA S.CREATININE B.SUGAR ECG BMI BWI LFT BS/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 above study as a subject. I have been informed to my satisfaction, by attending physician the purpose of clinical evaluation and the nature of the drug treatment. I also aware of my right 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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My commitment increases my level of energy. My energy increases my level of action. My action increases my level of success. My success increases my level of commitment.

Research in any field is the most important section of development. Ayurveda is in service is for ages to the needy mankind to relieve their ailments and recording the facts for the future generations. At present the Ayurveda research scholar, developing the Ayurveda and understanding under the limelight of contemporary scientific backgrounds. The plagiarism is more and more now a day in the scientific community. This is happening as the researches of the various institutions are not available for the common researcher. We wish to control this plagiarism by contributing the dissertations for scientific community. If you find any thesis is a copy of the previous publication, we take this issue to the university authorities for proper action. The solution to prevent copy cats is … http://ayurvedaresearch.wordpress.com/

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