Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
By
Dr.B.ARUN KUMAR.
B.A.M.S
GUIDE
2008
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
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.
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 am highly indebted to Dr.K. VijayaLakshmi, for her valuable suggestions being a co-
guide for my work.
I pay my sincere respect to Dr. M. Sadashiva Rao, principal of Dr. B.R.K.R Govt.
Ayurvedic College, Hyderabad for providing facilities for the research work.
I 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.
Place: Hyderabad
PART-A: Shaariram
Bibliography. 139
Annexure. 146
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.
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.
All most all surveys show that blood pressure rises with age in both men and
women. A national study showed that 76% of the male hypertensive and 88%of females
were in the age group of 25-60yrs.Framingham study showed that an average of 20-
mmofHg systolic and 10mmofHg diastolic increase from age 30-65yr.
Hypertension is one of the most important modifiable risk factors for coronary
heart disease in western and Asian population. Studies from India have shown an
increasing trend in the prevalence of hypertension. Community surveys have documented
that in a period of three to sex decades, prevalence of hypertension has increased about
30 times among urban dwellers and by about 10 times among the rural inhabitants. The
various studies estimated a prevalence rate of hypertension among urban population
ranging from 1.24%in 1949to 36.4%in 2003, and for rural people from 1.99%in 1958 to
21.21%in 1994. The sentinel surveillance project documented 28% overall prevalence of
hypertension (Criteria=JNCVI) from 10 regions of the country in the age group 20-69.
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.
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
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.
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.
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.,
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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
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.
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.
Humoral factors
Blood volume Constrictors Dilators.
-Sodium -Angiotensin II
-Prostaglandins
-Mineralo corticoids -Catacholamines -Kinins
*
-Atriopeptine -Thromboxane -NO/EDRF
-Leukotriens
-Endothelin
JG
Renin
Renin substrate
Angiotensin I
Angiotensin II
Sodium retention
BLOOD PRESSURE
*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.
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.
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.
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.
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”
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.
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-
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.
*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.
*Benign hypertension: Is moderate elevation of blood pressure and the rise is slow over
the years.
*Accelerated hypertension: Denotes a recent rise in blood pressure with retinal damage,
but without an papilla edema.
NIDANAM:
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 .
b) Viharaja:
1. Ativyayama, Vegasandharana, Vyavaya, Jagarana, Bharaharana,
Gajaturagaradha padhaticharya 8, Prapatana, Bhagnam.
c) Panchkarmajanya:
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.
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:
NIDANA REFERENCES:
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.
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).
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 .
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.
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 nerve-
endings to emotional sensory stress, and or increased reactivity of their arteriolar smooth
muscle to norepinephrine and epinephrine.
In some persons, the blood pressure increases due to the presence of the doctor
(white coat hypertension).this is possibly due to the temporary emotional stress. The over
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.
6)Meals:
After meals the blood pressure is little higher.
7)Emotions:
Rage and panic raise the blood pressure, however, in exceptional panic, there may
be fainting attacks.
8)Sleep:
Sleep causes a fall of blood pressure. However, sleep associated with nightmare,
dreams may cause rise of blood pressure.
9)Exposure to cold:
It causes rise of blood pressure. This is due to hypothalamic stimulation. There is
cutaneous vasoconstriction leading to increased resistance to the blood flow and elevation
of blood pressure (cutaneous vasoconstriction causes conservation of heat within the
body).
10)Geographic factors:
Several studies have shown that high altitude residents have lower blood pressure.
Possible constituting factors include-
1) Lower peripheral resistrance due to increased capillarisation of tissues.
2) Hypoxia causing reduced thyroid activity and
3) Primitive conditions.
11)Physical activity:
Several population studies have suggested that individuals who undertake regular
physical exercise have lower blood pressures than sedentary individuals.
12)Trace metals:
It has been claimed that both cadmium and lead; which are environmental
pollutants, may cause high blood pressure. The main source of cadmium to the human
body is cigarette smoke. Conversely, however, there is fairly good evidence that blood
pressures are lower in areas where the drinking water is hard (i.e, has higher calcium
content). The mechanisms for this are unknown.
13)Socio-economic status:
Blood pressure is consistently higher in people from the lower socio-economic
classes. The poorer classes have however, concurrently higher average body weight,
greater consumption of alcohol and tobacco and more exposure to noise etc., while some
studies in India have indicated a higher prevalence of hypertension in the higher socio-
economic groups, a very large study in Mumbai found no difference between high and
low socio-economic groups. So higher or lower socio-economic status does not have
significant effect on blood pressure.
14)Age:
The younger the patient when hypertension is first noted, the greater is the
reduction in life expectancy, if the hypertension is left untreated.
Older people tend to have higher blood pressure than young people. Almost all
surveys show that blood pressure rises with age in both men and women. Studies have
demonstrate the two important trends; firstly, blood pressure rises with advancing age
and secondly, those individuals whose blood pressure starts at a higher level tend to
retain their place in the distribution of blood pressure and therefore, sustain a faster age-
related rise in pressure. Due to thickening of vessel wall, as increase in sub-endothelial
layer and the media, which increase collagen content, elastic fragmentation and
calcification.
In vriddavasta vata is the predominant dosha. 17 there is high predisposition to
develop vataja vikaras in the old age. Physiological aggravation of vata with it ruksha,
khara, daruna, sheeta gunas etc., may cause sankocha and kathinyata of the vessels.
15)Sex:
At all ages and in both whit and non-white populations, females with
hypertension fare better than males up to the age of 65,and the prevalence of
hypertension in pre menopausal females is substantially less than that in age matched
males or post menopausal women. Yet, compared with their normotensive counterparts,
females with hypertension run the same relative risk of a morbid cardiovascular event as
males do.
Regarding the less prevalence of hypertension in premenopausal females, the
possible explanation in ayurveda is that female body is purified every month because of
menopausal flow (in the context of prameha nidana).
16)Smoking:
Nicotine and carbon monoxide, two major products of tobacco combustion, are
both potent vasoconstrictors. Tobacco smoking has been reported to cause acute rise of
blood pressure, but whether prolonged smoking leads to sustained hypertension has not
been established. Several studies from the developed world have reported no relationship
between smoking and levels of blood pressure; some have even reported slightly lower
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.
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
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.
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.
Disease Author
8
1.Pittaja kasa Astanga hridaya nidana
9
2.Pittaja hridroga 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
15
7.Pittaja chardi Madava nidana
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
9. Asta.hri.nidana-hridroga chap
10. Asta.hri.nidana-Trishna chap.
11. Madava nidana-Udavartha chap.
12. Asta.hri.nidana-madatyaya chap.
13. Madava nidana-madatyaya chap
14. Asta.hri.nidana-murcha chap
15. Madava nidana-chardi chap
16. Asta.hri.nidana-arshas chap
17. Madava nidana-arshas chap
18. Asta.hri.nidana-
19. Asta.hri.nidana-vidradi chap
20. Asta.hri.nidana-udaram chap
21. Madava nidana-udaram chap
22. Asta.hri.nidana-pandu chap
23. Madava nidana-pandu chap
24. Asta.hri.nidana-shopha chap
25. Madava nidana-shopaha chap
26. Asta.hri.nidana-visarpa chap
27. Madava nidana-visarpa chap
28. Sushri.sam.Nidana-Vata vyadi chap.
29. Madava nidana-krimi chap
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.
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.
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.
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.
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.
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.
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.
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.
started, the further vitiation of doshas takes place and land up into complication or
upadrava. This depends on the sthana or the organ that gets affected i.e., when mastishka
is affected, the condition or diseases like ardita, pakshagatha etc., are produced,it causes
drishti mandya etc., and when hridaya is affected, it causes hridroga etc.,
SAMPRAPTHI GHATAKAS:
1. Dosha- shariraka- vata- vyana, prana, udana
Pitta- pachaka, sadhaka
Kapha - avalambaka.
Manasika- rajas, tamas
Dosha prakopa
Agnimandhyam
Aamam
Saama doshas
Blood volume
Peripheral resistance
Hypertension
CLASSIFICATION OF HYPERTENSION:
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.
*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
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.
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.
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.
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.
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.
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.
9) G.Protein:
A recent study suggests that mutations in G.Proteins can lead to essential
hypertension.
Defects in renal
sodium hemostasis
Inadequate sodium
excretion
Cardiac Output
Total peripheral
resistance
Hypertension
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.
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
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.
DIFFERENTIAL DIAGNOSIS:
In modern science essential hypertension should be differentiated from secondary
hypertension. Following are the differentiating features.
COMPLICATIONS:(UPADRAVAS)
The occurrence of another disease in the wake of primary disease, as a
complication or sequel, is termed as upadrava (Madhukosha).
ORGAN COMPLICATIONS
ATHEROSCLEROTIC PRESSURE INDUCED
BRAIN Cerebralinfarction, Hypertensiveencephalopathy,
Transient ischaemic Cerebral haemorrhage,
attacks Lacunar infarcts
EYE 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, Aneurysms, aortic dissection.
ARTERIES Vascular occlusion.
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.
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.
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.
SBP ≤150
SBP ≥150 DBP ≤95
SBP ≤140 or orDBP ≥95 Continue to
SBP≥140 or DBP ≤90 Monitor
DBP≥90 Begin Begin Drug.
Continue to
Drug. Monitor
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;
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.
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.
PATHYA APATHYA
AHARA 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.,
All the drugs have vata, pitta hara and medhya properties. All the drugs are easily
available, non controversial and economical.
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.
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.
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
References:
1. Vanga sena- vata vyadhi prakarana
2. Bhava prakasha nighantu-3/1-10.
3. Dhanvantari nghantu 1/1-4,
4. Shodhala nighantu-1/96-98.
5. Cha.sam.Sutra-25/
Guduchi:
“Rasoguduchyaasthu samula pushpyah kalka prayojyah khalu shankha pushpyah
Aayuh pradhaanyamaya nashanaani balagni varna swara vardhanaani,
Medhyaani chaitani rasaayani medhyani vishesheenacha shankhapushpee”
(Cha.Sam.Chi.1.3.30-31)
2.APARAAJITHA:
Botanical name : Clitoria ternate
Family : Fabaceae
Synonyms : Aspotha, Gririkarni,Vishnukrantha, Swetha, Mahaswetha.
Properties:
RASA : Katu, Tikta, Kashaya
GUNA : Laghu, Ruksha
VIRYA : Sheeta
VIPAKA : Katu
KARMA : Tridosha hara, medhya, vishagna, chakshushya.
INDICATIONS : Kushta, shotha, unmada, vrana, shula.
PARTS USED : Root/Root bark; Seeds
DOSAGE : Root powder: 1-3gm.
Seed powder: 1-2gm.
Chemical constituents:
Aparajitin,tetraxerol,taraseron,alphaandbetasitosterols,robinin,quercitin,kaempfer
ol,ternatines A,B,C,D.It was mentioned in manasika rogas by raja marthanda.
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.
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.
Properties:
RASA : Tikta, Kashaya, Madhura
GUNA : Laghu, Snigdha
VIRYA : Sheeta
VIPAKA : Katu.
KARMA : Tridoshahara, Medhya, Balya, Kushtagna.
INDICATIONS : Kushta, Kandu, Visarpa, Jvara, Daha.
PARTS USED : Rhizome.
DOSE : powder: 1-3 gm.
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).
5.KARPAASA BEEJA:
Botanical name : Gossypium herbacium.
Family : Malvaceae
Synonyms : Tundikeri, swadanshtra.
Properties:
RASA : Katu
GUNA : Tikshna, Snigdha (Root bark-Laghu)
VIRYA : ushna
VIPAKA : Katu
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 .
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
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.
GUDUCHI APARAJITHA
SHATAVARI JATAMAMSI
GO GRITHAM
KARPASA
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.
CLINICAL STUDY:
My clinical study is “The effect of Karpasa beejadi Gritha Gutika” in the
management of Bhrama with special reference of Hypertension”.
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.
Inclusion Criteria:
(Based on “International Classification of Diseases -10”)
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.
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.
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.
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.
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:
1. INCIDENCE OF SEX:
1. Male 15 50%
2. Female 15 50%
Male
Female
2. INCIDENCE OF AGE:
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
3. INCIDENCE OF RELIGION:
Table No.3 Showing the incidence of Religion
1. Hindu 25 83.33%
2. Muslim 5 16.66%
Muslim,17%
1. Married 28 93.33%
2. Unmarried 02 6.66%
2; 7%
Married
Unmarried
28; 93%
5. INCIDENCE OF OCCUPATION:
Table No.5 Showing the incidence of Occupation in 30 patients of Hypertension.
2. Doctor 02 6.66%
3. Employ 09 30%
4. Labourer 07 23.33%
5. Students 01 3.33%
12
10
6
11
9
4
7
2
2
1
0
Housewife Doctor Employ Labourer Student
HIG, 2, 7%
LIG
MIG, 10, 33%
MIG
HIG
LIG, 18, 60%
1. Vegetarian 4 12.9%
2. Mixed 27 87.1%
Vegetarian, 6,
20%
Vegetarian
Mixed
Mixed, 24, 80%
8. INCIDENCE OF ADDICTIONS:
Table No.8 Showing the incidence of addictions.
2. Alcohol 03 10%
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%
14
12
12
10
8
6 5
4 4
4 3
2
2 1 1 1
0
l . .
g
ho ng w w w y. ns
y
in o i he he he dd io dd
he
w c ok C o t To
Al sm T. .C T.
C T di
c
C + +T + k+ ad
in
g co m
o
ok
dd
y o
ok ac S m No
b T. . Sm To T.S
Sm To l + T +
l + ho o.
o o lc
coh A
lc A
A l
1. Yes 14 46.66%
2. No 16 53.33%
16
14
12
10
No, 16
8 Yes, 14
6
4
2
0
Yes No
1. Fresh 10 40%
2. On medication 20 60%
20
On
Medication
10
Fresh
0 5 10 15 20
11.INCIDENCE OF HABITATE:
1. Town 19 63.33%
2. Rural 9 30%
3. Urban 2 6.66%
20 19
18
16
14
12
10 9
8
6
4 2
2
0
Town Urban Rural
2. Stage I 4 13.33%
3. Stage II 25 83.33%
25
25
20
15
10
4
5
1
0
High normal Stage I Stage II
1. Obese 11 36.66%
2. Non-Obese 19 63.33%
19
Non-Obese
11
Obese
0 5 10 15 20
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
12
10
10
8 7
6
6
4
4
2
2 1
0
Fresh 1mon- 6mon-1year 1yr-5yr 5yr-10yr 10yr-15yr
6months
15.INCIDENCE OF EDUCATION:
3 No Education 11 36.66%
14 13
12 11
10
8
6
6
4
2
0
Low education High education No education
16.INCIDENCE OF PRAKRITI:
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%
17.INCIDENCE OF STRESS:
1. No stress 4 13.33%
2. Psychological 19 63.33%
3. Psychological+Physical 7 23.33%
Physi+Psyco 7
stress 23.33%
19
Psychological 63.33%
stress
4
No stress 13.33%
0 10 20 30 40 50 60 70
1. Present 06 20%
2. Absent 24 80%
30
24
25
20
15
10
6
5
0
Present Absent
Table No.19 Showing the Incidence of patients using allopathic drug along with trial
drug in 30 patients of hypertension.
1. No drug 09 40%
3. Beta 5 16.66%
blocker+CCB
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%
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
RESULTS:
Results were assessed on the basis of clinical (Subjective parameter) as well as
Sphygmomanometer readings (Objective parameter) after the treatment.
BHRAMA
Table No.20
Total
Symptom ‘t’ ‘p’ Remarks
Grading Mean S.D. S.E. value value
Score x-x
Mean
SHIRAH SHULA
Table No.21
Total
Symptom ‘t’ ‘p’
Grading Mean S.D. S.E. value value Remarks
Score x-x
Mean
ANIDRA
Table No.22
Total
Symptom ‘t’ ‘p’
Grading Mean S.D. S.E. value value Remarks
Score x-x
Mean
Table No.23
Total
Symptom ‘t’ ‘p’
Grading Mean S.D. S.E. value value Remarks
Score x-x
Mean
1. Marked 11 36.66%
2. Moderate 14 46.66%
3. Mild 3 10%
4. No relief 2 6.66%
2, 7%
3, 10% Marked
11, 37%
Moderate
Mild
No relief
14, 46%
200
150
BT
100
AT
50
0
1 4 7 10 13 16 19 22 25 28
140
120
100
80 BT
60 AT
40
20
0
1 4 7 10 13 16 19 22 25 28
1. Marked 1 3.33%
2. Moderate 9 10%
3. Mild 14 46.66%
4. No response 6 20%
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.
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.
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.
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.
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.
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.
“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.
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 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.
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.
patient was not responded to the treatment even though he belongs to fresh group. Six
patients were belongs to the group “1month-6months”, in this group 3 patients were
responded mildly, two patients as moderately and one patient was not responded . One
patient belongs to the group of “6months-1 yr” chronicity was responded moderately.
Seven patients were belongs to the group of “1yr-5yr”chronicity, in this 5 patients
responded as mildly, one patient not responded. Four patients were belongs to the
chronicity group of “5yr-10 yr”, in this group one patient was responded as mildly, two
patients were responded as moderately, and one patient was not responded. In “10 yr-
15yr”group one patient was not responded and one patient was mildly responded.
After seeing all the chronicity groups, it was emphasized that all the chronic
sufferers of the hypertension were not responded well to the treatment. But, subjectively
all of them are relieved in symptoms satisfactorily.
Results according to deha prakriti,out of thirty patients twelve patients belongs to
VP prakriti, All the patients are responded in VP prakriti group. In this group, five
patients are mildly responded, five patients are moderately responded. Two patient were
not responded.
Seven patients belong to PK prakriti.Three patients improved mildly, one
patient was improved as moderately and three patients are not responded. Pittam has a
relation with rakta as ashrashrayi bhava relation. Pitta and Rakta prakopa may leads to
bhrama i.e., hypertension. Increase in sadrava pitta and rakta prakopa increase blood
volume in turn increases in cardiac output leads to hypertension. Increase in sadravapitta
leads to agnimandya then leads to ama formation.Which increases the viscosity of the
blood which increases peripheral resistance further leads to hypertension. This may be
the reason for the patients not responded in PK prakriti group.
Three patients belong to VK prakriti and three for KV prakriti, one patient
belongs to PV prakriti. In KP prakriti group also there is no marked improvement
patients. Only mild improved patients are three and one patient improved as moderately.
In VK prakriti group one patient is markedly improved, one patient was not
responded and one patient was mildly responded. In KV prakriti group on patient was
mildly improved, two patients were markedly improved.
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.
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.
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
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.
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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DR.B.R.K.R.GOVT.AYURVEDIC COLLEGE.
S.R.NAGAR, HYDERABAD-500038.
POST GRADUATDE DEPARTMENT OF KAYACHIKITSA.
S.No :
Name : Case : OP/IP
W/o d/o s/o: O.P.Regd.No :
Age : D.O.A :
Sex : D.O.D :
Occupation:
Address :
Income :
1 Chief complaint with duration:
2) Associated symptoms:
5) Treatment history:
7) Personal History:
Haibits :
Addictions :
Alcohol/Tobaccosmoking/Chewing/Toddy/Cannabis/Noaddiction.
Diet : Mixed/Veg.
Socioeconomic status:LIG/MIG/HIG
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 SAMHANANA
VIKRITHI AHARASHAKTHI
SAARA VYAYAMASHAKTHI
SATMYAM VAYAH
SATVAM PRAMANAM
g)Ashatastana Pariksha:
NADI SHABDHA
MALA SPARSHA
MUTRA DRIK
JIHWA AKRITHI
h)Srotopariksha:
RASAVAHA SHUKRAVAHA
RAKTAVAHA PRANAVAHA
MAMSAVAHA UDAKAVAHA
MEDHOVAHA ANNAVAHA
ASTHIVAHA SWEDAVAHA
MAJJAVAHA ARTAVAVAHA
FOLLOWUP:
INVESTIGATIONS 1ST 7TH 14TH 21ST 28TH 35TH 42ND 49 TH
DAY DAY DAY DAY DAY DAY DAY DAY
BP
CBP
CUE
BODY WEIGHT
LIPID PROFILE
ESR
B.UREA
S.CREATININE
B.SUGAR
ECG
BMI
BWI
LFT
BS/BP
Conclusion :
Result :
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: