A AYURVEDIC

APPROACH TO
CARDIOLOGY
Prof. Dr. S. N. Ojha
M.D. Ph.D (Ayu)

Director,
Post Graduate Studies
Yashwant Ayurved College Kodoli
Kolhapur

NEED OF THE HOUR

.

Expansion of Knowledge in Cardiac Ailments

considering the Ayurvedic Perspective
Evolution of Clinical diagnostic Criteria in
Ayurveda.
Modern Classified Cardiac diseases
correlation
in Ayurveda

Nirukti - Haraterete hrida shabda.

Shatapata Bramhana.
HRI-Aharan
- Venous Return
- Preload
DA-Danarthaka - Stroke Volume
- Afterload
YA-Gatyarthaka - Rhythmic Contractility - Contractility of
of Myocardium
Myocardium
& heart rate

A aerobic organ.
- Seat for oja
Indriya
atma
pranvayu

HRIDAYA

sadhak pitta
avalambak

kapha
mana

vyanvayu

- Rasavaha & Pranvaha moolasthan

Supply

demand

energy

workload

Dhamani - Supply nutrients oxygen for heart function

Vyan vata - dhatu poshak rasa vikshepan for hridayasta
dhatu karma.
Usnatva - causes stroto vishpar or vasodilatation and
maintain
abhivahan parampara.
Sheetatva - causes stroto rodha or vasoconstriction

Pranvahasrotas
Rasavahasrotas
Raktavahasrotas

Hridaya
Udakvahasrotas
Shonita kapha
prasadat
Srotamsi anya ca darunaihi

Contribution in pathogenesis of
Heart diseases
Epidemology
1.5 million people die of CVD every year.
2.4 million people suffer from IHD
India suffers the highest loss in potentially
productive years of life [ 35-64 years ]
By 2030, the loss is expected to rise to
17.9 million / year.
Prevalence of CVD is reported 2-3 times
higher in urban area than rural population.

Aetiology
A] Beej swabhavat sthula matapitrujanya
bhavat.
B] Previous exposure to behavioral risk

factors such as
i) Avyayam (Insufficient physical activity)
ii) Inappropriate nutrition
Diet deficient in fresh fruit, vegetables and
polyunsaturated fatty acids are associated
with an increased risk of vascular disease.

Charak has explained the role of shuska shaka,

shuska phala, teel, teelpalala, kshar katu anna to be
cause of gramya dosha and so hridroga.

Low levels of vitamin C, vitamin E and other

antioxidants

may

enhance

the

production

of

oxidized LDL.

Vrukshamla, dadima, matulunga are good source of

vitamin C and are so classified under Hridya gana.

Elevated

Homocysteine

level

confers

an

independent and incremented risk for vascular

disease.

Direct endothelial toxicity, failure of nitric oxide

release, smooth muscle cell proliferation, LDL
proliferation,

platelet

abnormalities,

abnormal

factor V, VII, vWF have been implicated.

Over cooking [vidagda aahar] destroys folic acid

from leafy vegetables a good source of folic acid.

Vidagda aahar causes rakta dusti has been

referred by our acharya.

Alcohol (Madya sevan) is antagonist to folic acid.

It is the cause explained in Raktapitta, Pandu,
Medodustikarak and a gramyadoshkar bhava.

Essential fatty acids are those that cannot be

synthesized by humans they can be derived
by food only.

Research has shown that diet rich in EFA

reduces serum cholesterol and LDL.

Coconut oil, Palm oil are low source of EFA

while Safflower oil, Sunflower Oil, Soyabean
Oil, Sesame Oil are relatively very good source
of linoleic acid, a important EFA.

Atisampurna aahar, guru, madhur snigdha,

pichchhil, paistik, anup mansa, varija mansa
are all high calorie diet.

Fat

consumption

expenditure

as

induces
most

is

very

little

stored.

energy

Meda

eva

upacheyate na tathe ittare dhatawa.

Cholesterol is found in all foods of animal origin.

The above hetu are responsible for dyslipidaemia.

Butter, Coconut oil, Palm oil are rich source of

saturated fatty acids which increase plasma
cholesterol.

Trans fatty acids render the plasma lipid profile

even more atherogenic than saturated fatty acids,
by not only elevating LDL cholesterol but also by

Trans fatty acids are high in concentration in

Deep fried fast food

Cake mixes
Cereal and Energy bars
Chips, Crackers and Whipped toppings
Packed Cookies and Candy
Packed doughnuts
Pies and Cakes.

Excessive Salt intake increase the incidence of

hypertension.

Upakledan, dosha sanchyanubanda, and its

action to bring shaithilyata to mansa and
shonita forms an important cause for Hridroga.

Angiopathy is a common complication of

diabetes

mellitus.

Insulin

resistance

is

associated with obesity and physical inactivity

as potent risk factor for CAD.

Various Hetu explained in concept of prameha

in sutrasthan 17th chapter hold the concept of
meda

vridhi

in

madhumeha

leading

to

hridroga.

Animal fat (anup, varija mansa) are low source

of Essential fatty acids. EFA decreases platelet

Antioxidant theory: Faulty dietary habits,

Exposure to carcinogen & sunlight,
Certain toxic drugs,
Cigarette smoking
Over exercise
All factors which increase free radicals.
1. These free radicals are short of electron
while in circulation through blood.
2. Antioxidant like vitamin A,C,E, neutralize
free radicals by donating their electron.
3. Hence diet low in vit. A,C,E and other
antioxidant are the cause of CVD.

What does gramya aahar

include?

Charak in Rasayan adhyaya has describe gramya aahar

to be consist of

Amla, lavana, katu, kshar pradhan aahar

Shuska shaka, shuska mansa, teel-tail & kalka and

ruksha content which have a very low nutritional value

Klinna, guru, pishtanna, adhyasana, avyayam and

abhishyandi aahar which are source of extra calories.

Virudha, asatmya, visham aahar, and paryushit anna

which have an impact on our immune system.

Day sleeping, Indulging in excessive exercise and sex,

Alcohol intake, which increases oxidation process and
release oxidants and free radicals.

Pshycological factors such as bhaya, krodha, lobha,

shoka, moha which are cause for the neuro-hormonal
imbalance, for example excess adrenaline secretion
and in turn over sympathetic activity.

General Symptoms
Vaivarya mrcch jvara ksa hikk vssyavairasya trr pramh|
chardikaphtkla ruj'rucicahrrdrgajsyurvividhstath'ny||
Ca.Ci.26/78

Discoloration in skin complexion

Chakrapani has mentioned that vaivarnya etc are seen after hridroga
has been manifested or in some cases they are presenting symptoms
on basis of which hridroga is manifested.
1. Cyanosis is general presentation in cardiac diseases
2. Lupus pernio, pink discoloration on the tip of nose, face etc which is
generally a feature of sarcoidosis wth cardio-pulmonary involvement.
3. Livedo
reticularis, is characterized by mottled, erythematous
discoloration of the skin, which blanches on pressure. It is is the most
common dermatologic manifestation of a cholesterol embolism.
4. Erythema
marginatum is a flat to mildly elevated, pinkish,
nonpruritic, transient eruption found primarily on the trunk and
proximal extremities. It occurs in 10% of children with their first
attack
of
acute
rheumatic
fever
(ARF).

. Xanthelasma is Yellow flat plaques over the upper or

lower eyelids, most often near the inner part of the
eye. It is seen in a patient with hyperlipidemia.
Eruptive xanthomas are characterized by crops of 1- to
5-mm yellow-orange papules with surrounding
erythema, most commonly on the extensor surfaces
of extremities and the buttocks. This condition is
most strongly associated with hypertriglyceridemia.
Conjunctival pallor; Pallor in a patient with a prosthetic
valve may be indicative of hemolytic anemia.
Osler's nodes are associated with subacute bacterial
endocarditis and S viridans. Osler's nodes are
painful, erythematous nodules most commonly
found on the pulp of fingers and toes.
Other cutaneous manifestations of infective
endocarditis include splinter/subungual
hemorrhages.

Fainting/ Murcha (Syncope):Cardiac syncope may be due to

arrhythmias or structural cardiac diseases that cause a decrease in
cardiac output leading to acute global impairment of cerebral blood
flow.
Fever
Cough/ Hiccup/ Dyspnea: It is caused due to cardio-pulmonary
relationship.
Anorexia/ Unpleasant taste in mouth:
1. Cardiac disease of any cause can cause hepatic dysfunction through
elevated hepatic vein pressure (congestive hepatopathy), decreased
hepatic blood flow (ischemic hepatitis), or hypoxemia. Further cardiac
dysfunction can lead to secondary renal injury through reduced renal
blood flow (low cardiac output), renal venous congestion (elevated
CVP), and impaired renal autoregulation. In both the organ (liver and
kidney) injury alongwith anemia caused due to cardiac disorders
anorexia and unpleasant taste is the common feature.
2. It may also be noted that anorexia nervosa can complicate in heart
disease. As patients with anorexia lose weight, they lose muscle mass,
both of the skeletal and cardiac type. When patients lose cardiac
muscle mass, they can develop mitral valve prolapse. This can give
the symptom of sharp pain beneath the sternum.

Excess thirst: The extra fluid in the body may cause

increased urination, particularly at night which can lead
to increase thirst [trishna].

Confusion/unconsciousness

Cardiac vomiting [chardi]: Left ventricular receptors

which appear to signal intramyocardial tension cause
bradycardia and vasodilatation, and increase urine flow.
They are probably important in blood volume control and
in adjusting the circulation during exercise.
When strongly stimulated they cause nausea and reflex
vomiting.
They may be involved in the autonomic disturbances at
the onset of myocardial infarction, syncope in aortic
stenosis, vasovagal syncope, and fluid retention in
heart failure.

Distress/pain/

Samanya Samprapti of Hridroga

dayitv rasa d vigu hrrdaya gat
kurvanti hrrday bdh hrrdrga ta pracakat ||
Su Ut. 43/4
Dalhan Commentary
kupit d hrr dayagatv rasa dayitv
hrr day bdh kurvanti, ta hrr drga
pracakat II
Aggravated d vitiates the rasa and hampers the
functional activity of hridaya leading to hridroga.
The pathogenesis takes place as mentioned in the
next slide.

Pathophysiology Considering CVD

Hriths
hool

Dhamani pratichaya
- common in area where rheological forces
act.
Factors responsible for genesis of Dhamani
pratichaya
1) sama meda
2) Vyan vata
3) injured dhamani or strotas.

Sama meda
mahabhuta)

Kledatva ( enriched in prithvi & aap

altered ratio between dravatva & ghanatva.

Pratighata &

Vyan vata due to

apratighata.
pratighat.

Vyan vata due to

pratighat.

vyan vata (rheological forces)

on srotas

exerts pressure

Injury to strotas (Kha vaigunya)

vata stimulates
Pratighatv
a
beneath
srotas

sama
medha
having
sanga
property

Proliferation of anu srotas

( Sandhankara :
sharirasya
garbhaa Kritinam

contribute to dhamanipratichaya/
atherosclerosis

Vyan vata unable to supply according to

demand
Supply

demand.

disparity
Apatarpan & dhatu kshaya in
hridayasthan

Role of Grathita Rakta

Kaphanubande Rudhire Sa Pitte Kanthagate Syad Grathite
C.Chi 4/93

Not Only Reduced Supply But Also Accumulation of end Metabolites in

cells lead to IHD
Samanavruta apana

Impaired
saman
Supply
&
agnivyapar

Due to
avrita
Apana
Intermediates Metabolites
are not excreted from
Cardiac Cells

IHD
dipaniyaghrita (omega - 3 fattyacid.)

Avrita vyan
vata
dhatu poshak
rasa
in hridaya sthan

Kitta of dhatu
metabolism do not
come out & retain in
hridayasta anu
strotas
impairs dhatu poshan

Coronary Atherosclerosis
Dhamani
Thrombosis

Hridayasta
Pratichaya
Grathita Rakta

Narrowing Of coronary
Artery
Myocardial Ischaemia
Apatarpana

Srotosanga/Avarodha

(Hridayastha)

Chest Pain
Vataprakopa
I.H.D.

Hrithshool(Chest Pain)

Vatika Hridroga:
Etiology /Causative Factors / Sadhyo Nidan
vyymatktivirkabasticintbhayatrsagadticr|
chardymasandhraakarannihrrdrgakartrr
r itath'bhightaII
Ca.Ci.26/77

Excessive physical exertion

Excessive exercise/ exertion explain the increase demand on already
compromised heart.
Drastic and excessive administration of purgation and enema therapies
Tikshna and excessive virechan and basti which will induce loose motions in
excess will reduce water content leading to reduce fluid volume and
blood pressure.
Thus to maintain the blood pressure heart will need to pump blood but due
to reduce fluid volume the heart may unable to pump or if the heart is
already compromised excessive workload will not be barred by the heart.
Further loss of fluid volume due to tikshna virechan and basti can also
cause electrolyte imbalance leading to arrhythmia and hence heart
disease.

Excessive anxiety/worry, fear, stress

Chinta bhaya explain the adrenaline influx which causes

tachycardia which may again lead to heart disease in
a compromised heart.

Faulty management of diseases

Gada atichara here means faulty management of disease

for eg patient is suffering from severe ama atisara,
already there is fluid loss and without considering the
bala of patient if vaidya does not give medicine to
stop the motion since there is sama avastha the
patient may collapse at any given moment.

Suppression of vomiting and ama (products

improperly digested),
Emaciation and
Trauma(physical and mental).

Kalantar Nidan:

kpavsavyymarkauklpabhjanai [1]
vyurviya hrrdaya janayatyuttam rujamII
[Ca.Su.17/30]
grief,
fasting,
excessive exercise,
intake of unctuous food,
dry and
inadequate quantities of food,

For understanding of modern diseases in

Ayurveda, IHD
& vatik hridroga are correlated herewith as
parameter.
Nidana of vatik hridroga Risk/Precipitating factor
of IHD
Rogaatichar/ rogatikarshan Hypertension
Ativyayam

Excessive physical activity

Shoka, Chinta, Bhaya

Excessive Emotions

Adhyashan

Heavy meals

Dhoomrapana

Smoking

vpathurvana stambha pramha nyat

dara[2]
hrr di vttur rpa jr ctyarthavdan||
Ca.Su.17/31

Tremors
Excruciating pain, cramps,
stiffness,
Feeling of darkness/ getting blank,
feeling of sense of emptiness,
Worsening of pain after the digestion of food

hrrcchnyabhva drava a
bhda
stambhsamhpavandvi
a|

Feeling of emptiness in the cardiac region

palpitation/tachycardia,
dryness of cardiac muscles
(wasting/atrophy),
pricking pain,
obstructed movement (heart block)
mental confusion (unconsciousness)

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

11.

Vata is necessary for the coordinated functioning of heart.

If vata gets vitiated the conduction defects may occur.
Tachycardia and bradycardia are the 2 main classification of impaired cardiac
conduction.
Dara or dardarika as explained by Chakrapani or hridrava as explained by
Yogindranath Sen explained the tachycardia.
Various rhythmic and arrhythmic tachycardia have been described by Modern
science for eg.
Sinus tachycardia
Atrial fibrillation
Atrial flutter
AV nodal reentrant tachycardia
Accessory pathway mediated tachycardia
Atrial tachycardia
Multifocal atrial tachycardia
Junctional tachycardia
Ventricular tachycardia
Any narrow complex tachycardia combined with a problem with the
conduction systemof the heart, often termed "supraventricular tachycardia
withaberrancy",
A narrow complex tachycardia with an accessory conduction pathway, often
termed "supraventricular tachycardia with pre-excitation" (e.g.
WolffParkinsonWhite syndrome).

Hridstambha explains the bradycardia.

Stoppage, obstruction, suppression are various
meaning of stambha.
Sinus bradycardia,
Sick sinus syndrome,
AV block etc explain the condition of slow heart
rate.
Asystole, also known asflatline, is a state of no
electrical activity from theheartand therefore
no blood flow. It results incardiac arrest.
It may also be noted that tachycardia may later
convert into asystole.
Thus various condition resulting into tachycardia
and bradycardia may be considered in vataja
hridroga.

Near-fainting or fainting (murcha), Dizziness,

Confusion or memory problems (pramoha/
sammoha) are the symptoms other then chest
pain, Fatigue, Shortness of breath.

Hritshunyata explains the emptiness due to

non filling of the heart chambers as
desolateness is also meaning of sunyata or it
may be understood as akinesia wherein no
movement (asystole) is observed.

ANGINA
THE ENGLISH WORD ANGINA REFERS TO
A PAINFUL CONSTRICTION TIGHTNESS
SOMEWHERE IN THE BODY
AND MAY REFER TO :
ANGINA PECTORIS
ABDOMINAL ANGINA
LUDWIGS ANGINA
PRINZMETALS
ANGINA
VINCENTS ANGINA
ANGINA
TONSILLARIS

Angina pectoris, commonly known as

angina, is severe chest pain due to
ischemia (a lack of blood and hence
oxygen supply) of heart muscle, generally
due to obstruction or spasm of the
coronary arteries.

The term derives from the Greek ankhon

(Strangling) and the Latin Pectus
(chest), and can therefore be translated
as a strangling feeling in the chest.

hrr itshula (Angina) pathogenesis

kaphapittvaruddhastu mrut rasamrcchita
hrrdistha kurut lamucchvsrdhaka
param sa hrrcchla iti khyt
rasamrutasambhava Su. Ut. 41/131-132
Kapha, pitta or both when impedes the gati of
vata which is associated with rasa especially
in cardiac muscles leads to chest pain
(hritshoola/ angina).

As there is deficiency of nutrition to cardiac

muscle against demand of cardiac muscle
leads to angina.

Role of psychological factors in Hritshula

In panduroga increase loading on hridaya precipitate Hridayashoola

Hridayagata Vata - Vridha Vata Impairing function of

hridaya
Aortic Stenosis
Left Ventricular Outflow obstruction
C.O
Contractility of Myocardium
of Left Ventricle
LVH
Demand = Supply
Angina Pectoris
Hridayagatavata.

Chest discomfort

Symptoms

the discomfort is usually described as a pressure,

heaviness, tightness, squeezing, burning, or choking
sensation.,
Anginal pains may also be experienced in the epigastrium,
back, neck, jaw, or shoulders, following skin dermatomes.
It is typically precipitated by exertion or emotional stress.
It is exacerbated by having a full stomach and by cold
temperatures.
Pain may be accompanied by breathlessness, sweating
and nausea.
It lasts for about 3 to 5 minutes, and is relieved by rest or
specific anti-angina medication.

Subtypes
Stable angina is typically presented as
chest discomfort and associated
symptoms precipitated by some activity
(running, walking etc.) with minimal or
non-existent symptoms at rest.
Unstable Angina
It occurs at rest (or with minimal
exertion), usually lasting > 10 min;
it is severe and of new onset (i.e., within
the prior 4-6 weeks);
it occurs with a crescendo pattern (i.e.,
distinctly more severe, prolonged, or
frequent than previously).

Diagnosis
Electrocardiogram (ECG)
Exercise ECG Test (Treadmill Test)
Thallium Scintigram
Stress Echocardiography
Coronary Angiogram

Differential Diagnosis

Differential diagnosis of chest pain has been

mentioned just after krimija hridroga. Relationship
exists
between
krimi,
annavahasrotas
(gastrointestinal tract) and heart disease.
Ca. Vi. 7/12 explains that diet like milk, sesame,
fish etc leads to kaphaja krimi which have origin in
amashaya
(gastrointestinal
tract)
and
hridaychara a type of kaphaja krimi can cause
chest discomfort.
Chest pain explained in verse 100-103 of
Trimarmeeya chikitsa adhyaya is of non cardiac
origin.

bhukt'dhikajryatilamalpajrsthitac
tII

If chest pain increases just after food intake

and demises during digestion and relieved on
empty stomach it is kapha dominant.

jr'dhiklam II

If pain aggravates during digestion it is pitta

dominant .

yadijryatisyt lam II

If pain increases after digestion on empty

stomach it is vata dominated.

Hritrujam in vataja Gulma aggravated after

completion of digestion & relieved by intake of
food.
Hridroga shanka - Pain experienced in anxious
person (Heenasatwa) at precardiac area
mentioned in grahani, udavarta
Koshtagata vikara should be taken in
consideration for D/D
Shoth starts from pedal parts indicate cardiac
disease.

Some features differentiating cardiac from Non-cardiac

chest pain
Favoring Ischemic Origin
Ischemic origin

Against

1.Character of Pain
Constricting
Squeezing
Burning
Heaviness, heavy feeling

Dull ache
Knife Like,Sharp
stabbing,jabs
Aggravated Respiration

2. Location of Pain
Substernal
In the left submamary area
Across Mid Thorax,
In the Left hemithroax
Anteriorly
In both arms, shoulders
In the Neck, Cheeks, Teeth's
In the Forearms, Fingers
In the interscapular region

Some features differentiating cardiac from Non-cardiac chest

pain
Favoring Ischemic Origin

Against Ischemic

origin
3. Factors Provoking Pain
Exercise
Pain after completion of exercise
Excitement
Provoked by a specific body motion
Other forms of Stress
Cold Weather
After Meals

Stable angina pectoris usually develops gradually with

exertion, emotional excitement, or after heavy meals.
Chest discomfort due to esophageal reflux is worsened
by post prandial recumbency and relieved by antacids .
So is the case with gall bladder disease wherein chest
discomfort may follow meal.
Chest discomfort due to peptic ulcer is relieved with

Pittaj Hridroga

Umla lavaa kra kaukjrabhjanai|

madya krdhtapaicu hrrdi pitta prakupyati||
Ca. Su. 17/32
intake of hot, sour, salty, alkaline (caustic) and
pungent foods,
taking food during indigestion,
excess of alcohol,
anger,
exposure to Sun
Hetu like lavana excess explains the rakta vikrut
vridhi which leads to hypervolaemia contributing
to hypertension and thereby hypertensive cardiac
disease.

Lakshana of Pittaj Hridroga

Pittt tamdyana dha mh santrsa tpa
jvara ptabhv||Ca. Ci.26/79
Darkness of vision/blackout: The cardiogenic
shock leads to cardiac syncope (tamo
darshan/ moha) and giddiness,
burning sensation/ heat sensation: Acute
pericarditis present as pain as if burning
sensation (daha).
confusion/unconsciousness,
Distress The myalgia due to infection leads
to distress (satras).

Pyrexia: In tuberculous pericarditis, fever,

night sweats (sweda), and weight loss, are
commonly noted.
Yellowishness: Breakdown of haemoglobin may
also be the cause for yellow discoloration
alongwith hepatic involvement
A small number of patients present with
fulminant myocarditis, with rapid progression
from a severe febrile (jwar) respiratory
syndrome to cardiogenic shock that may
involve multiple organ systems, leading to
renal failure, hepatic failure (cause for pittata),
and coagulopathy.

hrr ddhastiktat vakr tiktmldgiraa klama|

trr mrcch bhrama svda
pittahrr drgalakaam || Ca.Su.17/32-33

heartburn,
bitter taste in the mouth,
eruptions with bitter and sour taste,
exhaustion,
thirst,
unconsciousness,
dizziness,
Perspiration.

1.

2.
3.
4.

Pittaj hridroga includes infective

conditions of cardiac diseases like
infective endocarditis/ myocarditis/
pericarditis,
Rheumatic heart disease,
infective cardiomyopathy.
Alcohol, chemotherapeutic drugs, heavy
metals like arsenic etc induced heart
disease has similarity with pittaj
hridroga.

Kaphaja Hridroga:
atydna gurusnigdhamacintanamacanam|
nidrsukha cbhyadhika
kaphahrrdrgakraam || Ca. Su.17/34
Excessive intake of food,
Intake of heavy and unctuous food,
Inadequate mental exercise,
Sedentary habits,
Excessive sleep

stabdhagurusytstimitacamarma
kaphtpraskajvaraksatandr|
Bradycardia,
heaviness
timidity of heart /dullness
associated with salivation,
Fever,
cough and
Drowsiness

hrrdaya kaphahrrdrg supta

stimitabhrikam|
tandrrucipartasya bhavatyamvrrta
yath||
[Ca.Su.17/34-35]
Bradycardia,
lesser activities of heart,
stiffness and
heaviness of the heart,
drowsiness and
anorexia.
The patient feels as if his chest is loaded with
stones.

Stabdha, Sputa and Stimita are the 3 lakshana

mentioned by Caraka.
The Sanskrit meaning of the word stabdha is
firmly fixed, stiff, rigid, immovable, paralyzed,
senseless, dull, solidified, tardy, slack, slow
Whereas supta means insensible, dull, resting
, latent, inactive
Stimita means fixed, rigid, unmoved,
motionless, steady; paralysed, flowing gently
along.
It means heart is motionless, inactive, slow,
solidified, rigid, these 3 words extent the
scope of kaphaja hridroga from non infective
cardiomyopathy to cardiac tamponade.

Pulseless electrical activity(PEA), also known by as

electromechanical
dissociation,
refers
to
cardiac arrestin which a heart rhythm is observed on
the electrocardiogram that should be producing apulse,
explains the supta; Chakrapani says niskriyata is the
meaning of supta.
The stretching of myocardium is reduced resembles the
stabdhata.
Due to collection of fluid the steady motionless
condition wherein the apex beat is not palpable or
peripheral pulse is not palpable explains stimitata
Pulseless electrical activity leads to a loss of cardiac
output, and the blood supply to thebrainis interrupted.
As a result, PEA is usually noticed when a person
loses consciousness (suptata) and stopsbreathing
spontaneously.
The cool touch resembles stimitata and the heaviness
felt is ashmavrita.

Sannipatik hridroga
vidyttridatvapisarvaliga||Ca. Su. 26/80
All of the previously mentioned symptoms of all
the three dosa are manifested together.
This type of heart disease is caused by the
combined vitiation of all the three doa.
This can be diagnosed by the existence of the
various signs and symptoms of all the three
types of heart diseases.
This type of heart disease is very painful and
difficult to cure.

Krr mija Hridroga

tvrrtitdakrrmijasakam

There is intense discomfort/acute pain and

piercing pain with itching.
In heart disease caused by the vitiation of all
the three doa, if one consumes Tila Sesame
(Sesamum indicum Linn), milk, sugar candy,
etc. this causes nodules in the heart. Rasa
becomes sticky in some parts of the heart. This
stickiness produces pathogenic organisms.
Symptoms like as if heart is being pierced or
being cut into pieces by weapons.
There is itching and pain in the heart.

Congenital cause (sahaja) of Valvular disease

Vitiate tridosha.
Sannipatik hridroga
with intake of
krimija aahar
Krimija hridroga.
In CHD Secondary Infective Endocarditis may arise
(Krimija hridroga)

Hridroga Samprapti
Agnimandyak
ar Nidan
Aama
Aamavisha

Doshprakop
Nidan

Khavaigunya
kar Nidan

Sanchaya

Rasavaha
Strotasa
Vaigunya

Dhatudaurbalyak
ar Nidan
Rasadhatwagni
becomes upahata

Prakopa

Sansrishtena
Prasar

Vyadhi Virodhikatwa
and
pratibandhakatwa
Bala hani

Aamavisha
Rasanugata
Rasa dhatu
becomes sheethila
Sthana
sanshraya
in the moola of
rasavaha
Srotas, Hridaya

Doshdushya
sammoorchhana
Cont

Sanga dushti

Atipravruti dushti

The haani of
vikshepan
Karma of
vyanavata

The hyper
functioning of
hridaya koshas

Hani of
Poshan
Of Hridaya
koshas
(apatarpan of
koshas)

Aati visfarana
(dilatation)
of hridayasth
Mansapeshi
Hridvridhi
(cardiomyopathy)

Again vata
Vridhi

Siragranthi
dushti
Deposition of
aama in
hrithkapata
Vikriti of
hrithkapata
Pranvaha and
rasavaha
strotodushti
janya
Vikara
Rheumatic
heart diseases

Vimargagaman
Dushti
Pranavaha
strotodushti
janya
Vikara
Backward
transmission
and pressure
from Left heart
to lungs
Pulmonary
hypertension
C.H.F.

Hrithshool
(I.H.D)

Guru, Snigdha, Madhur

Sama annarasa
Dushayanti rasam
Meda eva upachiyate
(Excessive Adipose Accumulation)
Fat Free Mass
Systemic
Vascular

Sthaulya
Resistance

Sleep Apnea/ Obesity

dhatavo na
Hyperventilation Syndrome
bhavati

Aavruta margatvat eva shesha

aapyayante atyartha ato alpa prano

to fulfill
the demand
Pranvahasrotodushti

L V Stroke Volume
Contd.

contd.
No change in heart
rate
Shwas
Pulmonary Arterial HTN

Cardiac Output
Hridayam badha Kurvanti

Dosha Hridayam

Gatva

R V H & Enlargement

RVF
(Hridroga)

LV Enlargement
Hypertension
L V Wall Stress
Hridayam badha

kurvanti
LVH
LV Systolic Dysfunction

LV Diastolic

Dysfunction

L V F (Hridroga)

Congestive Cardiac Failure

(marmopaghata)
Cirrhosis
Pregnancy
Cardiac Output
Vasodilatation

Peripheral
Vikar vighata bhava
Non Osmotic Vasopressin Release
Vasopressin V2 Receptor

Aquaporin- 2
Increased water permeability of collecting duct
Bahya Sira Prapya
Water Retention

Shoth

Marmoghata

Left VentricularFailure

Right Ventricular Failure

IHD
Myocarditis
Valvular Heart Disease
Restrictive Pericarditis

Cor Pulmonale
Right sided Valvular Disease
Right sided Myocardial Disease
Pulmonary Hypertension

Compensatory Mechanism (Vikar Vighat Bhava)

Activation of Norephinephrine
Atrial natrouretic peptide
vridhi

Activation of RAAS

Myocardial Contractility
Vata
Cardiac

workload
Tachycardia

Cell Stretching
(vyas is among vata vridhi

lakshana)
Further stress on myocardium (Vikar Vighat abhav)
Compensatory
Hypertrophy
CCF
Dilatation

&

Types of Heart Failure

Low-Output Heart Failure

Systolic Heart Failure:
decreased cardiac output
Decreased Left ventricular ejection fraction
Diastolic Heart Failure:
Elevated Left and Right ventricular end-diastolic
pressures
May have normal Left ventricular ejection fraction
High-Output Heart Failure
Seen with peripheral shunting, low-systemic
vascular resistance, hyperthyroidism, beriberi,
carcinoid, anemia
Often have normal cardiac output
Right-Ventricular Failure
Seen with pulmonary hypertension.

Types of Heart Failure

Systolic Dysfunction
Coronary Artery Disease
Hypertension
Valvular Heart Disease
Diastolic Dysfunction
Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy
(HCM)
Restrictive cardiomyopathy

HYPERTENSION

HTN is a major risk factor for the development

of CVD.
Arbitary definition of HTN in adults aged 18
years and older who are not acutely ill, is
defined as Systolic blood pressure (SBP) of
140mm of Hg or greater and/or diastolic blood
pressure (DBP) of 90mm Hg or greater or any
level of blood pressure in patients taking
antihypertensive medications

Risk Factors

A) Non modifiable risk factors

Age
Sex
Genetic factors
Ethnicity
B) Modifiable risk factors
Obesity
Salt intake
Saturated fat
Alcohol
Reduced Dietary fiber
Heart Rate
Physical inactivity
Environmental Stress
Socio Economic Status
Oral Contraception

Hypertensive emergency
Ahypertensive emergency(Systolic over 180 or diastolic over
120)
(formerly
called"malignant
hypertension")
is
hypertension with acute impairment of one or more
organ systemsthat can result inirreversibleorgan damage.
(especially thecentral nervous system, cardiovascular system
and/or therenal system)
Causes

discontinuationof antihypertensive medications

autonomic hyperactivity

collagen-vascular diseases

drug use (particularly stimulants, especiallycocaineand

amphetaminesand theirsubstituted analogues)

Glomerulonephritis

Head trauma

Neoplasias,

PreeclampsiaandEclampsia

Renovascular hypertension

Progressive or impending end-organ dysfunction.

Sign & Symptom

Neurological Cardiovascul
ar

Renal

other organ systems

hypertensive myocardial isc

encephalopath hemia
/infarction
y
,

acute
renal failure
or
insufficiency

retinopathy

Epistaxis,
Dyspnea

cerebral vascu
lar accident
/
cerebral infar
ction
subarachnoid
,
hemorrhage

acute left
ventricular
dysfunction

eclampsia

acute
pulmonary
edema

microangiopat Vomiting
hic
hemolytic an
emia

intracranial
hemorrhage

aortic
dissection

Severe
anxiety

Paresthesias

Agitation

Altered
mental status

Pathophysiology

1. Abrupt increase insystemic vascular resistance

, likely related to humoralvasoconstrictors
2. Endothelialinjury
3. Fibrinoid necrosisof thearterioles
4. Deposition ofplateletsandfibrin
5. Breakdown of normal autoregulatory function
6. The resultingischemiaprompts further release
of vasoactive substances, completing a
vicious cycle.
7. If the process is not stopped, a vicious cycle of
homeostatic failure begins, leading to loss of
cerebral and local autoregulation, organ system
ischemia
and
dysfunction,
and
myocardial infarction.

Aortic Stenosis
Aortic stenosis(ASorAoS) is the narrowing of the exit of theleft ventricleof
theheart.

It may occur at theaortic valveas well as above and below this level.
Causes

include being born with abicuspid aortic valve

rheumatic fever

Old age

Risk factors:smoking,high blood pressure,high cholesterol,diabetes, and

being male.
[[[]

Symptoms:

decreased ability to exercise often occurring first

loss of consciousness (syncope) typically occurs with standing or exercise

heart related chest pain (Angina) occurs due to AS the outcomes are worse
Signs of heart failure:

shortness of breath especially whenlying down,at night, or with exercise

swelling of the legs

"Dresden china" appearance ofpallorwith a lightflush

heart murmur

Pathogenesis
Increased age
Abnormal

Classical Cardiovascular Genetic

Risk Factors HTN,
SMOKING etc

Predisposition

Haemodynamic
Forces
Calcium

Lipid
Metabolism
Dhatukshaya
Kha vaigunyakar
(meda)
Janya vata prakopa
dhatvagni mandya

Bija dushti

Vyan vayu dushti

(asthi)

elevated strech & shear

stress
Endothelial Cell Remodelling
asthivridhi

Endothelial Cell Injury

meda

sama

(Vikar Vighat Bhava)

Nodules are formed at the margin of cusps
accumulation (adsorption)
& later extends throughout
Valvular interstial cell
of bone related proteins
proliferation
such as osteopontin
Aortic stenosis
of LDLc

osteoblast

osteoblastic differentiation

Aortic
Valve Calcification
cells

calcium deposition
on collagen scaffold

stimulate

accumulation

formation of foam

pro-inflammatory factors

Aortic Stenosis

Systolic murmur
S2 Loud
Ejection Sound
Lt. Ventricular Out flow Obstruction
Sanga
C.O.

Bhrama, Aayasena Shwas

Vimargagaman
Pranavaha Srotodushti
Shwasadi

Lt. Ventricular hypertrophy

Demand
Hridayagata

vaata
Chest pain

Diagnosis
Pulsus Parvus et tardus: Slow and/or sustained upstroke of the arterial
pulse, and the pulse may be of low volume.
Apical-carotid delay: Noticeable delay between thefirst heart sound(on
auscultation) and the corresponding pulse in thecarotidartery.
In a similar manner, there may be a delay between the appearance of
each pulse in the brachial artery and the radial artery.
The first heart sound may be followed by a sharp ejection sound
("ejection click") best heard at thelower left sternal borderand the
apex, and, thus, appear to be "split".
An easily heardsystolic, crescendo-decrescendo (i.e., 'ejection')murmur
is heard loudest at the upper right sternal border, at the2nd right
intercostal space,and radiates to thecarotid arteriesbilaterally.
The murmur increases with squatting and decreases with standing and
isometric muscular contraction such as theValsalva maneuver, which
helps
distinguish
it
fromhypertrophic obstructive cardiomyopathy
(HOCM).
The second heart sound (A2) tends to become decreased and softer as
the aortic stenosis becomes more severe.
One may hear afourth heart sounddue to the stiff ventricle.
When dilatation of the ventricle will occur, a third heart sound may be
manifested.

Other peripheral signs include

sustained, heavingapex beat,which is not displaced unless
systolic dysfunctionof theleft ventriclehas developed

Aprecordial thrill

narrowed pulse pressure

ECG

Manifestations ofleft ventricular hypertrophypattern (LVH)

are common in aortic stenosis

Rarely include ECG patterns characteristic of certain types of

heart blocksuch asLeft bundle branch block.
Xray

showing the degree of calcification of the valve, and in a

chroniccondition, an enlarged left ventricleand atrium
Echocardiogram

increased pressure gradient, and these parameters are used

to classify and grade the aortic stenosis as mild, moderate or
severe

may also show left ventricular hypertrophy, thickened and

Mitral stenosis
Mitral stenosisis avalvular heart diseasecharacterized by
the narrowing of the orifice of themitral valveof theheart.
Signs and symptoms:

Heart failuresymptoms,
such
asdyspnea on exertion,
orthopnea andparoxysmal nocturnal dyspnea(PND)

Palpitations

Chest pain

Hemoptysis

Thromboembolismin later stages when the left atrial

volume is increased (i.e. dilation). The latter leads to
increase risk ofatrial fibrillation, which increases the risk of
blood stasis. This increases the risk of coagulation.

Ascitesandedemaand
hepatomegaly
(if
right-side
heart failuredevelops)

Fatigue and weakness increase with exercise and

pregnancy

Causes:

Secondary torheumatic fever

Congenital heart disease
Infective endocarditis
Cleftmitral valve: It is the most common valvular heart
disease inpregnancy
Other rare causes:
Mitral annular calcification
Endomyocardial fibroelastosis
Malignant carcinoid syndrome
Systemic lupus erythematosus
Whipple disease
Fabry disease
Rheumatoid arthritis
Hurler' disease
Hunter's disease
Amyloidosis.

Mitral Stenosis
SI Loud

Lt. Ventricular Diastolic Murmur

Inflow obstruction Opening Snaps

Sanga

Vimargagaman

Pranavahastrotodushti

Shwas, Kasa, Raktasthivan etc.

Cardiac Output

Rasavikshepana

Apatarpana

Bhrama (Giddiness)
Shaitya (cold Extremities)
Heen Nadi (Low Volume Pulse)
Shyavata (Cyanosis) etc.

Mitral Regurgitation S1 Soft

Systolic Murmur
Mitral Valve
Incompetence

Vimargagaman

Pranavahastrotodushti

Shwasa, Kasa, Raktasthivan etc.

Hridayadushti (R.H.F.)

Vimargagaman
Rasavaha, Raktavaha Strotodushti

Shotha
Yakriddalyudar
Jalodar
JVP (Siranamayam)

Diagnosis

Thefirst heart soundis usually loud

Tappingapex beat

Ifpulmonary hypertensionsecondary to mitral

stenosis
is
severe,
the
P2(pulmonic)
component of thesecond heart sound(S2) will
become loud.

An opening snap that is a high-pitch additional

sound may be heard after the A2(aortic)
component of the second heart sound (S2).
A
mid-diastolic
rumblingmurmurwith
presystolic accentuation will be heard after the
opening snap.

Other peripheral signs include:

Malar flush- due to back pressure and buildup of
carbon dioxide (CO2).
Atrial fibrillation- irregular pulse and loss of 'a'
wave in jugular venous pressure
Leftparasternal heave- presence of right
ventricular hypertrophy due to pulmonary
hypertension
Medical signsofatrial fibrillationinclude:
Heart rate is about 100-150/min.

Irregularly irregular pulse with a pulse deficit>10.

Varying first heart sound intensity.
Presystolic accentuation of diastolic murmur
disappears.
Embolic manifestations may appear

Chest X-ray: showsleft atrial enlargement.

Electrocardiography
P mitrale: that is, broad, notched P waves in
several or many leads with a prominent late
negative component to the P wave in lead V 1,
and may also be seen inmitral regurgitation,
and, potentially, any cause of overload of the
left atrium.
Echocardiography
shows left atrial enlargement, thick and calcified
mitral valve with narrow and "fish-mouth"shaped
orifice
and
signs
of
right ventricular failurein advanced disease.
decreased opening of the mitral valve leaflets,
and increased blood flow velocity duringdiastole

Pran Avrit Udana

(Avrit
(Avrit
))

Uda
Uda
na
na

(Avaraka)

Pran Vayu

Prayatn
Prayatn
a
a

Urdhwa
Urdhwa
Gati
Gati

Varna
Varna

Urja
Urja

Udan
Udan
aa
Karm
Karm
aa
Bala
Bala

Udana
Udana karma
karma hampered
hampered due
due to
to
avarana
avarana of
of Prana
Prana
mis
mis matching
matching
Sangraha
Sangraha of
of nishwas
nishwas and
and uchshwas
uchshwas
Failure
Failure of
of control
control over
over immune
immune System
System
Auto-immune
Auto-immune Disorders
Disorders

Rheumatic
Allergic
Rheumatic Heart
Heart disease
disease
Allergic
Rhinitis
Rhinitis
(Hridroga)
(Shiroroga/
(Hridroga)
(Shiroroga/
Pratishyay)
Pratishyay)

Pran
Pran Avrit
Avrit Udana
Udana

Treatment
Treatment

Ashwasana
Ashwasana Chikitsa
Chikitsa

Saman
Saman Avrit
Avrit Apan
Apan

(Avrit
)

Apa
na

(Avaraka)

Samana Vayu

Saman
Saman Avrit
Avrit Apan
Apan
Agnisand
Agnisand
h-ukshan
h-ukshan

Muncha
Muncha
n
n

Vivecha
Vivecha
n
n

Saman
Saman
a
a
Karma
Karma

Dharan
Dharan

Pachana
Pachana

Saman
Saman Avrit
Avrit Apan
Apan
Due
Due to
to vitiated
vitiated Saman
Saman Vayu
Vayu
The
The No.
No. of
of intermidiete
intermidiete
dharan
dharan
Metabolite
Metabolite inceases
inceases
ItIt Obstruct
Obstruct the
the Gati
Gati
Of
Of Apan
Apan Vayu
Vayu
Ischemia
Ischemia
moves
moves
(Hridoga)
(Hridoga)

Begins
Begins

Unable
Unable to
to
Apakwa
Apakwa ahara
ahara
Grahani
Grahani

Apakwa
Apakwa ahara
ahara
forward
forward

Parshwashool
Parshwashool

Samana
Samana avrit
avrit Apana
Apana

Treatment
Treatment
Agnidipak
Agnidipak Ghrita
Ghrita

Apan
Apan Avrit
Avrit Vyan
Vyan

(Avrit
)

Vyan
a
(Avaraka)

Apan Vayu

Apan
Apan Avrit
Avrit Vyan
Vyan
Apana
Apana Vayu
Vayu
Restrict
RestrictGati
Gatiof
ofVyan
Vyanvayu
vayu
between
between
Atipravrutti
Atipravrutti
Vyan
Vyan
Mutra
MutraPurisha
PurishaRetasa
Retasa
of
of
Avrita
Avritato
to

karma
karma
reduced
reduced

Interplay
Interplay
Gati
Gatiof
ofApan
Apan&&

Srijan
Srijankarma
karma&&gati
gati
Apana
Apanavayu
vayu
Vyan
Vyanvayu
vayu
Rasavikshepan
Rasavikshepan
Of
OfVyan
Vyanvayu
vayu

Apan
Apan Avrit
Avrit Vyan
Vyan
Diarrhoea
Diarrhoea

Dehydration
Dehydration

Decrease
Decrease ventricular
ventricular feeling
feeling
Heart
Heart rate
rate &
& Vasoconstriction
Vasoconstriction (Peripheral)
(Peripheral)
Dehydration
Dehydration
Cardiac
Cardiac Output
Output
Reduced
Reduced Rasavikshepana
Rasavikshepana

Hypovolumic
Hypovolumic shock
shock

Apan
Apan Avrit
Avrit Vyan
Vyan

Treatment
Treatment

Sangrahan
Sangrahan

Vyan
Vyan Avrit
Avrit Udana
Udana

(Avrit
)

Vyan
(Avaraka)

Udana Vayu

Vyan
Vyan Avrit
Avrit Udana
Udana
Paroxymal
Paroxymal Tachycardia
Tachycardia
Abnormility
Abnormility in
in the
the different
different portion
portion of
of Heart
Heart
(( Atria/
Atria/ Purkinj
Purkinj Fiber/
Fiber/ ventricles)
ventricles)
Rapid
Rapid Rhythmic
Rhythmic discharge
discharge of
of impules
impules
Spread
Spread in
in direction
direction
throught
throught the
the Heart
Heart
Re-entrant
Re-entrant Pathway
Pathway
Causes
Causes ischemic
ischemic
Damage
Damage

Vyan
Vyan Avrit
Avrit Udana
Udana

Continue
Continue
There
There is
is never
never co-ordinate
co-ordinate contraction
contraction of
of
ventricular
ventricular muscles
muscles at
at once
once which
which is
is
required
required
for
for cardiac
cardiac pumping
pumping
Causes
Causes

Dizziness
Dizziness
Fatigability
Fatigability

Dypsnoea
Dypsnoea
(Bala
(Bala ,, Prayatna
Prayatna Reduced)
Reduced)

AYURVEDIC APPROACH TO PRIMARY

& SECONDARY PREVENTION OF IHD
& HTN
A)

Aaharatmak

1. Aaharmatra punaha agnibala

apekshani
2. Prakritim anupahatya
3. Yatha kalam jaram gachathi
4. Aahar matra Sarvagraha
Parigraha
5. Aahar prakriti anurupa dwividha
prakar
guru na agni sandukshan,

6. Dravya apekshaya tribhaga sauhityam

ardhasauhityam va gurunam upadisyate na

ati sauhityam agneyuktyartham laghunaam
api
7. Matravat ashanam anupahatya bala varna
sukhayusha
8. Guru pishtamaya na khadet matram
bubhukshit
9. Shuska mansa, shuska shaka, shaluka,
bisa, krisa, mansa, kurchika,
kilata, shaukar, gavya, mahisha mansa,
matsya, dadhi, masha, yavaka
na shilayet- ahita aahar sevan- dhatu
sanghat nashayati

10. Shastik shali, mugdha, saindhava,

aamalaki, yava, antariksha jala, sarpi,
jangala mansa, madhu abhyasayet
11. Aahar aachar chestashu sukharthi
pretya ca iha ca
param prayatnam tisted bhudhiman
hita sevane
Ca. SU. 7/
60
12. Ahita aahar upayoga punaha vyadhi
nimittam iti
Ca. Su. 25/30
13. Virodhi annapana nisheda
Aama
dosha karaka
14. Aahar vidhi visheshayatana

Prudent Diet:

Varied eating pattern should be followed

Preference to fish, chicken, low fat dairy
products
Salt & alcohol intake should be moderate
Consume more unrefined carbohydrates
such as grains product.
Antioxidants like amalaki, lemons,
spinach, turnip leaves, watermelon,
sweet potatoes, carrots, tomatoes,
pumpkin, wheat grass juice, oranges,
guava, should be added in diet.

B) Viharatmak
Vyayama nitya sevan
sharira chesta ya chesta sthairyartha
balavardhini
Deha vyayama sankhyata matraya tam
samacharet
Ca. Su. 7/32
Ativyayama nisheda
Vyayama hasya, bhasya adhwa
gramyadharma prajagaran
Nichitan api sevan bhudhiman ati matraya
Ca. Su. 7/34
Avoid Smoking
Prevent stress
Follow aachar rasayan

Qualities of some important food item

Oryza sativa Research shows dietary

supplementation with anthocyanin rich extract
prevented development of fructose induced
insulin resistance.

It lowers oxidative stress and it improves certain

metabolic abnormality associated with diets
high in fructose

Mung - Its polysaccharides composition

enhances enzyme activity, serum lipoprotein
LDL levels of TG hydrolysis to reach curative
effect of lowering blood fat

It contains globulin and polysaccharides, it can

promote animal cholesterol in liver bile acid,
accerelate decomposed into bile salts in the bile
secreted and reduce absorption of cholesterol
small intestine.

Yava (Hordeum vulgare) It lowers

LDL and total cholesterol levels. Study
shows it has beneficial effect on lipid
metabolism and bowel function.
Maricha (Piper nigrum) Piper nigrum
can increase absorption of selenium vit. B
and beta carotene and curcumin as well
as other nutrients. It has antioxidant
properties.
Patola (Trichosanthes dioca) Water
extract shows it reduces fasting blood
glucose, pp blood glucose, aspirate
amino transferase, alanine amino
transferase, alkaline phosphatase,
creatinine, urine sugar and urine protein
It has antioxidant potential and antiinflammatory activity.

Karvellaka (Momordica charantia) It

reduces liver secretion of Apolipoprotein B the
primary lipoprotein of LDL and also reduces
Apoliporotein C the primary lipoprotein of VLDL
and increase expression of apolipoprotein A-1
the primary component of HDL. It also stimulate
insulin secretion from pancrectic cells.
Kulatha (Dolichos biflorus) It has
antioxidant activity, hydroxyl radical scavenjing
reduces lipid peroxidation. It has hypolipidemic
activity and lowers blood sugar level.
Ushira (Vetiveria zizanioides) It shows
antioxidant properties. It scavenges free radicals
Banana (Musa paradisiaca) contain dietary
fibre, high amount of essential minerals,
potassium, vit. A, B1, B2 & C. It has soluble fibre
which binds with bile salt and may reduce blood
cholesterol levels

Kusmanda (Benincasa hispida) antioxidant

property, scavenging free radicals
Dadima (Punica granatum) antioxidant,
protect body from free radicals. It reduces LDL and
increase HDL
Shampaka Shaka (Aragvad patra) - It reduces
blood sugar level and has antioxidant activity and
also reduces blood and liver total lipids
Mulak (Rapharus sativus) improve blood
circulation. It lowers plasma levels of total
cholesterol, TG, phospholipids. It also shows
hypoglycemic activity.
Eranda taila (Ricinus communis) - Ricinoleic
acid exerts anti-inflammatory effects
Draksha (Vitis vinifera) - study shows it relieves
symptoms of chronic venous insufficiency,
arteriosclerosis and high blood pressure, alleviate
inflammatory conditions and is cardioprotective.

MEDICINE

A multiple direction approach should be

kept in treatment of CVD & HTN.
Causative factors and the pathology
should be understood than only
treatment should be started.
Role of sama meda, rasa-raktavaha and
pranvaha srotas, vata dosha, grathita
rakta, hridaya kriya, satva,
rogatikarshana, all these factors should
be considered and then multidrug
combination should be decided.

Drugs acting on amashit

meda

Maricha
Chitrak
Daruhari
dra
Rason
Tulsi
Vacha

Pushkarmool
a
Punarnava
Shilajeet
Triphala
Amrita

Musta
Pippali
Kutki
Drugs explained
in Urustamba,
sthaulya and
santarpanotha
vyadhi chikitsa
can be chosen.

Drugs acting on grathita rakta

Kamalkshar

Utpalnal kshar

Darbha

Kusta

Paravatashakri

Asana
Role of katu
rasa pradhan
dravya should
be studied
since Charak
says it has
shonita
sanghata
bhinnati
action.

Mrinal

Palash kshar

Priyangu kshar

Drugs acting on Rasa Raktavaha

srotas

Amalaki
Haritaki
Punarnav
a
Shatavari
Shalparni
Sariva
Manjista

Shilajeeta
Amrita
Yastimadh
u
Patola
Kutki
Vidanga
Laksha

Drugs acting on Pranvaha

srotas

Vasa
Amrita
Punarnava
Amalaki
Pushkarmool
a
Kusta
Kachora
Kantakari
Brihati

Lagupanchamool
a
Somvalli
Haridra
Daruharidra
Bharangi
Yastimadhu
Pippali
Mrigashringa

Drugs acting on Vata

dosha

Dashamoo
la
Haritaki
Rason
Guggulu
Punarnava
Shalparni

Shatavari
Pushkarmoola
Deodaru
Mrigashringa
Nagbala

Drugs having Medhya

action

Brahmi
Sankhapushpi
Jatamansi
Guduchi
Yastimadhu
Shatawari
Haritaki
Brahmarasayan

Drugs having mutrala effect so

reducing the hypervolaemia

Punarnav
a
Gokshur
Musta
Ushir
Dashmula
Varun

Pashan bheda
Brahmi
Padmak
Pundarik
Madhuk

Drugs having Hridya Effect

Arjun
Brahmi
Tulsi
Guggulu
Punarnava

Rason
Shatawari
Amalaki
Yastimadhu

Kalpa

Hridayarnav Rasa
Dadimadya Ghrita
Navayas churna
Prabhakar vati
Arjunarista
Hartone
Arjin
Cardomac

Role of shodhan karma

Shodhan karma in hridroga has its own limitation.

It should be ordered considering the basic

parameters, cardiac preload, afterload, age etc.

If preferred mridu prayog should be carried out

that too of virechana.

Yapana Basti can be reassured.

Snehan should be preferred with

polyunsaturated fatty acids.

Tikshna swedan should not be done

mainly in IHD as peripheral circulation
increases and central circulation is
reduced further increasing the ischaemia

Shirodhara, Shirobasti, Hridbasti,

Raktamokhsana have their own limitation
and should be preferred as and when
required.

DOUBTS??

Thank you