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Throughout history, diseases of the heart have captured the concern and interest of
investigators. Ancient Greek and Roman physicians observed the serious and often fatal
consequences of heart disease. But effective treatment for heart disease was limited to
rest and painkillers until the eighteenth-century discovery of the therapeutic properties of
the foxglove plant, whose dried leaf is still used to make the medicine digitalis.

The Middle Ages ,The emphasis in medieval Europe on suffering as an experience of

spiritual growth did not bode well for research concerning the heart. However, advances
were made by Arab scholars, whose culture encouraged scholarly research. The medical
writing of Ibn Sina, known as Avicenna (980-1037), included a rich sampling of astute
observations about heart disease. This book was translated widely in the East and West
and was highly influential for centuries. Although he repeated some of Galen's errors
about the heart, Avicenna also distinguished between many types of heart disease,
including those caused by a wound or abscess, those caused by collapse of the heart, and
those caused by an obstruction in the heart. In the thirteenth century, Ibn Nafis challenged
soAIn 1775, William Withering (1741-1799), a British physician and botanist, was called
to evaluate a folk remedy for dropsy, a serious condition involving an accumulation of
fluid in the body that can affect the heart, the liver, and other organs.Contemporary
physicians use foxglove, now called digitalis, to boost the strength of heart contractions
and to lower the heart rate. It is often used in cases of congestive heart failure but can be
used for other types of heart disease as well. Withering realized the potential danger in
using too much foxglove and warned in 1785 that too much of the

The open heart ,For most of medical history, the heart was seen as untouchable, limited
by the difficulty of operating on the organ that kept the body alive. An 1896 book about
chest surgery by Stephen Paget noted that "surgery of the heart has probably reached the
limits set by nature to all surgery." stretching the artery by using a plastic balloon which
is inflated when the tube is in the coronary artery. A total of 399,000 angioplasty
procedures were performed in 1992, according to the AHA.AAA The most dramatic
change in treatment of heart disease was the development of methods to replace the most
damaged hearts with healthy human hearts or even animal hearts. The first successful
human heart transplant was performed by South African surgeon Christiaan Barnard in
1967. The patient, however, died in 18 days. Though many surgeons tried the operation,
success was limited, most patients dying after days or months, until the early 1980s,
when effective drugs were developed to fight organ rejection. In 1993, a total of 2,300
heart transplants were performed in the United States, where the one-year survival rate is
81.6%, according to the AHA.

Finally William Harvey, a pupil of Hieronymus Fabricius (who had earlier described the
valves of the veins without recognizing their function), performed a sequence of
experiments and announced in 1628 the discovery of the human circulatory system as his
own and published an influential book about it. This work with its essentially correct
exposition slowly convinced the medical world. Harvey was not able to identify the

capillary system connecting arteries and veins; these were later described by Marcello
Malpighi Throughout history, diseases of the heart have captured the concern .
William Harvey 1628:
Demonstrated blood flow in one direction through blood vessels thus discovered blood
Marcello Malpighi 17th century:
Observed capillaries through the microscope thus discovered anatomical link between
arteries and veins


The cardiovascular/circulatory system transports food, hormones, metabolic wastes, and

gases (oxygen, carbon dioxide) to and from cells. Components of the . A cardiovascular
system in biology classes is an organ system that moves substances to and from cells; it
can also help stabilize body temperature and pH. There are three types of circulatory
systems (from simplest to most complex): no circulatory system, open circulatory system,
and closed circulatory system.

Open circulatory system

An open present in some invertebrates like simple mollusks and arthropods in which
circulatory fluid in a cavity called the hemocoel (also spelled haemocoel) bathes the
organs directly and there is no distinction between blood and interstitial fluid; this
combined fluid is called hemolymph (also spelled haemolymph). Muscular movements
by the animal during locomotion can facilitate hemolymph movement, but diverting flow
from one area to another is limited. When the heart relaxes, blood is drawn back toward
the heart through open-ended pores.Hemolymph fills all of the interior hemocoel of the
body and surrounds all cells..system is an arrangement of internal transport

Closed circulatory system

The main components of the circulatory system are the heart, the blood, and the blood
vessels.The circulatory systems of all vertebrates, as well as of annelids (for example,
earthworms) and cephalopods (squid and octopus) are closed, meaning that the blood
never leaves the system of blood vessels consisting of arteries, capillaries and
veins.Arteries bring oxygenated blood to the tissues (except pulmonary arteries), and
veins bring deoxygenated blood back to the heart (except pulmonary veins). Blood passes
from arteries to veins through capillaries, which are the thinnest and most numerous of
the blood vessels.. This is known as single circulation the four-chambered heart of birds
evolved independently of that of mammals.

Mammalian circulation

Poorly oxygenated blood collects in two major veins: the superior vena cava and the
inferior vena cava. The superior and inferior vena cava empty into the right atrium. The
coronary sinus which brings blood back from the heart itself also empties into the right
atrium. The right atrium is the larger of the two atria although it receives the same
amount of blood. The blood is then pumped through the tricuspid, or atrioventricular,
valve into the right ventricle. From the right ventricle, blood is pumped through the
pulmonary semi-lunar valve into the pulmonary trunk. This blood leaves the heart by the
pulmonary arteries and travels through the lungs (where it is oxygenated) and into the
pulmonary veins. The oxygenated blood then enters the left atrium. From the left atrium,
the blood then travels through the bicuspid valve, also called mitral or left atrioventricular
valve, into the left ventricle. The left ventricle is thicker and more muscular than the right
ventricle because it pumps blood at a higher pressure. Also, the right ventricle cannot be
too powerful or it would cause pulmonary hypertension in the lungs. From the left
ventricle, blood is pumped through the semi-lunar valve into the aorta. Once the blood
goes through systemic circulation, peripheral tissues will extract oxygen from the blood,
which will again be collected inside the vena cava and the process will continue.
Peripheral tissues do not fully deoxygenate the blood, thus venous blood does have
oxygen, only in a lower concentration in comparison to arterial blood. The release of
oxygen from erythrocytes is regulated. decrease in pH. Such characteristics are exhibited
by tissues undergoing high metabolism, as they require increased levels of oxygen. The
autonomic nervous system is widely distributed throughout the body and controls a
variety of bodily functions, including blood pressure and heart rate. The efferent
peripheral autonomic nervous system is composed of two opposing subsystems, the
sympathetic nervous system and the parasympathetic nervous system.

Components of the vascular system include:

blood: consisting of liquid plasma and cells

Distribution of Blood:
Minor circuits within systemic circulation arranged in parallel carrying blood to each
organ of the body

Resting cardiac output approx 5 L/min distributed between the major organs as follows:

Brain 0.75 L/min

Heart Muscle 0.25 L/min

Gastrointestinal 1.5 L/min


Kidneys 1.0 L/min

Skeletal Muscle 1.0 L/min

Skin 0.5 L/min

blood vessels (vascular system): the "channels" (arteries, veins, capillaries) which carry
blood to/from all tissues. (Arteries carry blood away from the heart. Veins return blood to
the heart. Capillaries are thin-walled blood vessels in which gas/ nutrient/ waste exchange

heart: a muscular pump to move the blood

There are two circulatory "circuits": Pulmonary circulation, involving the "right heart,"
delivers blood to and from the lungs. The pulmonary artery carries oxygen-poor blood
from the "right heart" to the lungs, where oxygenation and carbon-dioxide removal occur.
Pulmonary veins carry oxygen-rich blood from tbe lungs back to the "left heart."
Systemic circulation, driven by the "left heart," carries blood to the rest of the bo the
sytem from the digestive organs into the portal vein. Waste products are removed by the
liver and kidneys. All systems ultimately return to the "right heart" via the inferior and
superior vena cavae.
A specialized component of the circulatory system is the lymphatic system, consisting of
a moving fluid (lymph/interstitial fluid); vessels (lymphatics); lymph nodes, and organs
(bone marrow, liver, spleen, thymus). Through the flow of blood in and out of arteries,
and into the veins, and through the lymph nodes and into the lymph, the body is able to
eliminate the products of cellular breakdown and bacterial invasion.

Adults have up to ten pints of blood. Forty-five percent (45%) consists of cells - platelets,
red blood cells, and white blood cells (neutrophils, basophils, eosinophils, lymphocytes,
monocytes). Of the white blood cells, neutrophils and lymphocytes are the most
important. Fifty-five percent (55%) consists of plasma, the liquid component of blood


Anatomy of the Heart:

Location and Size:

Located behind the sternum, resting on the diaphragm, near middle of the thoracic cavity.
Apex - points to the left side of the body
Base - wide upper posterior margin of the heart

Great Arteries:
Pulmonary Trunk - carries deoxygenated blood from right ventricle to lungs
Aorta - carried oxygenated blood out of the left ventricle. Arteries branch from the aorta
to organs of the body
Great Veins:
Superior and Inferior Vena Cava - returns deoxygenated blood from head and trunk to
the right atrium

Pulmonary veins - carry freshly oxygenated blood from lungs to left atrium

Heart Chambers and Valves:

The four chambers - four separate chambers in the heart

Atria - Right Atrium - deoxygenated blood from body

Left Atrium - deoxygenated blood from lungs

Ventricles - Right Ventricle - deoxygenated blood to lungs

Left Ventricle - oxygenated blood to body

Four Valves:-
There are four one way valves in the heart

Atrio-ventricular (AV) valves - connect atria and adjacent ventricles

Bicuspid (left AV/Mitral valve) - left atrium and ventricle

Tricuspid (right AV valve) - right atrium and ventricle

Chordae Tendineae:-
AV valves flexible to be pushed open by small force (pressure difference in atrial and
ventricular blood is less than 1 mm Hg)

Withstand high pressures generated when ventricles contract

Prevent eversion of the valve during ventricular contraction - reflux of blood back into

Papillary muscles:
Located on inner surface of ventricles, regulate tension in chordae tendineae

Semi Lunar Valves:

• Aortic Valve - separates left venrtricle from aorta
• Pulmonary Valve - separates right ventricle form pulmonary trunk

Backflow of Blood:

Following ventricular contraction, ventricles relax and pressure drops suddenly.

Pressure in aorta and pulmonary artery drops more slowly.

Arterial pressure almost immediately exceeds intra-ventricular pressure. One way valves
prevent back-flow of blood into the heart

Heart Tissue:
Cardiac Muscle:-
Branched, cylindrical, striated fibres (cells) containing one or two centrally located nuclei

Branched Fibres - cardiac muscle fibres form a network. Smooth spread of impulse

Intercalated Discs - unique to cardiac muscle; irregular transverse thickenings of plasma

membrane, contain desmosomes and gap junctions

Desmosomes - hold adjacent cells together (spot welds), located lateral borders of
adjacent cells

Gap Junctions - small cytoplasm filled channels, allows impulse to pass quickly to
neighbouring cells

A double layered membrane surrounding the heart. Formed by invagination of pericadial
sac during 4th week of embryonic development

Fibrous Pericardium (outer layer) - tough heavy connective tissue, protects against
over extension during vigorous exercise

Upper fuses with great vessels entering the heart

Lower rests on diaphragm

Serous Pericardium (middle layer) - two layers

1 Parietal Layer - fused to fibrous pericardium
2 Visceral Layer - adheres tightly to heart muscle,
part of heart wall (epicardium)
Pericardial Cavity - fluid filled space between 1-2

Heart Wall:
Three layers:
Epicardium - thin transparent membrane attached to myocardium
Myocardium - thick portion of heart wall, myofibres (cardiac muscle cells)
Endocardium - Inner lining of the heart, endothelial cells continuous with lining of
great vessels

Heart Conduction System:

Specialised group of cardiac muscle cells designed for starting each heart contraction and
co-ordination of spread of contraction

Components of System:
Sinoatrial node - SA node, pacemaker, small mass of cells embedded in wall of right

Spontaneous depolarization 100 time per minute

Activity modified by autonomic nerves to 75 times per minute at rest

Atrioventricular node - AV node

Atrioventricular bundle - AV bundle, Bundle of His

Right and Left Bundle Branches

Conduction Myofibres - Purkinje Fibres

Sequence of Excitation:-

Precise co-ordination is crucial to ensure blood flow through the heart

1. SA node depolarizes - special fibres transmit impulse right → left atrium

2. Atria contract - excitation spreads from upper regions downwards

• Non conducting fibrous ring blocks conduction between atria and ventricles
• AV node slows down the speed of electrical transmission. 0.1 sec delay gives atria
time to finish contracting before ventricles contract
• AV node connects with Bundle of His and carries impulse to bottom of ventricles
• Bundle branches into smaller myofibres (Purkinje fibres), radiate upwards into

Lower ventricular muscle contracts - pushes blood towards aortic and pulmonary

Middle and Upper ventricular muscle contracts - squeezes blood into Aorta and
pulmonary artery

The anatomy of the heart can be conveniently be divided into five functional units:

o The heart muscle (the 2 atria pump blood into the ventricles and the 2
ventricles pump blood out of the heart)
o The valves of the heart which maximize the pumping action of the heart (2
atrioventricular valves: the tricuspid and mitral; 2 semilunar valves: the
pulmonic and aortic)

o The electrical pacemaker and conduction system which sets the normal
rhythym of the heart and coordinates the contraction of the heart
(sinoatrial (SA) node, atrioventricular (AV) junction, His bundle, Purkinje

The coronary circulation which distributes blood to the heart

The autonomic nervous system innervation of the heart which regulates heart rate and
contractility (sympathetic nerve endings in muscle of atria and ventricles, SA node, and
AV junction; parasympathetic nerve endings mainly in atrial muscle, pacemaker, and the
AV junction

Arteries, veins, and capillaries comprise the vascular system. Arteries and veins run
parallel throughout the body with a web-like network of capillaries connecting them.
Arteries use vessel size, controlled by the sympathetic nervous system, to move blood by
pressure; veins use one-way valves controlled by muscle contractions.

Arteries are strong, elastic vessels adapted for carrying blood away from the heart at
relatively high pumping pressure. Arteries divide into progressively thinner tubes and
eventually become fine branches called arterioles. Blood in arteries is oxygen-rich, with
the exception of the pulmonary artery, which carries blood to the lungs to be oxygenated.

The aorta is the largest artery in the body, the main artery for systemic circulation. The
major branches of the aorta (aortic arch, ascending aorta, descending aorta) supply blood
to the head, abdomen, and extremities. Of special importance are the right and left
coronary arteries, that supply blood to the heart itself.

The arterioles branch into the microscopic capillaries, or capillary beds, which lie bathed
in interstitial fluid, or lymph, produced by the lymphatic system. Capillaries are the
points of exchange between the blood and
surrounding tissues. Materials cross in and out of the

by passing through or between the cells that line the

capillary. The extensive network of capillaries is
estimated at between 50,000 and 60,000 miles long.1

Blood leaving the capillary beds flows into a series of
progressively larger vessels, called venules, which in turn unite to form veins. Veins are
responsible for returning blood to the heart after the blood and the body cells exchange
gases, nutrients, and wastes. Pressure in veins is low, so veins depend on nearby muscular
contractions to move blood along. Veins have valves that prevent back-flow of blood.

Blood in veins is oxygen-poor, with the exception of the pulmonary veins, which carry
oxygenated blood from the lungs back to the heart. The major veins, like their
companion arteries, often take the name of the organ served. The exceptions are the
superior vena cava and the inferior vena cava, which collect body from all parts of the
body (except from the lungs) and c

Arteries and veins have the same three tissue layers, but the
proportions of these layers differ. The innermost is the intima;
next comes the media; and the outermost is the adventitia.
Arteries have thick media to absorb the pressure waves created by
the heart's pumping. The smooth-muscle media walls expand
when pressure surges, then snap back to push the blood forward
Blood vessel anatomy when the heart rests. Valves in the arteries prevent back-flow. As
blood enters the capillaries, the pressure falls off. By the time blood reaches the veins,
there is little pressure. Thus, a thick media is no longer needed. Surrounding muscles act
to squeeze the blood along veins. As with arteries, valves are again used to ensure flow in
the right direction. hannel it back to the heart.


General survey of cardiovascular system and physical principles. Introduction to

cardiovascular system - Heart, blood and vessels, systemic and pulmonary circuits,
physical principles - pressure, flow (laminar and turbulent), resistance, viscosity,
haematocrit, radius, vessels.

The cardiovascular system consists of a pump (the heart), which pushes a complex fluid
(blood) around a closed system of tubes (blood vessels). For the heart and brain survival
time without blood is minutes, and storage capacity of tissues for O2 is low.
Cardiovascular disease is the biggest killer in the western world and includes
hypertension, stroke, atherosclerosis and ischaemic heart disease.

Cardiovascular Physiology

Introduction Systemic circulation

The heart Blood flow: Hagen-Poisseuille formula
Electrophysiology of the heart Control of systemic circulation
Cardiac cycle Control of arterial pressure
Coronary circulation Cardiovascular responses to anaesthesia
Cardiac output

The cardiovascular system consists of the heart and two vascular systems, the systemic
and pulmonary circulations. The heart pumps blood through two vascular systems - the
low pressure pulmonary circulation in which gas exchange occurs, and then the systemic
circulation, which delivers blood to individual organs, matching supply to metabolic
demand. Blood pressure and flow is largely controlled by the autonomic nervous system
The Autonomic Nervous System, Update in Anaesthesia 1995;5:3-6), and is also
influenced by surgery and anaesthetic drugs. A good working knowledge of
cardiovascular physiology is necessary topractice safe anaesthesia.

The heart comprises four chambers, and is divided into a right and left side, each with an
atrium and a ventricle. The atria act as reservoirs for venous blood, with a small pumping
action to assist ventricular filling. In contrast, the ventricles are the major pumping
chambers for delivering blood to the pulmonary (right ventricle) and systemic (left
ventricle) circulations. The left ventricle is conical in shape and has to generate greater
pressures than the right ventricle, and so has a much thicker and more muscular wall.
Four valves ensure that blood flows only one way, from atria to ventricle (tricuspid and
mitral valves), and then to the arterial circulations (pulmonary and aortic valves). The
myocardium consists of muscle cells which can contract spontaneously, also pacemaker
and conducting cells, which have a specialised function.

Electrophysiology of the heart Myocardial contraction results from a change in voltage

across the cell membrane (depolarisation), which leads to an action potential. Although
contraction may happen spontaneously, it is normally in response to an electrical impulse.
This impulse starts in the sinoatrial (SA) node, a collection of pacemaker cells located at
the junction of the right atrium and superior vena cava. These specialised cells depolarise
spontaneously, and cause a wave of contraction to pass across the atria. Following atrial
contraction, the impulse is delayed at the atrioventricular (AV) node, located in the septal
wall of the right atrium. From here His-Purkinje fibres allow rapid conduction of the
electrical impulse via right and left branches, causing almost simultaneous depolarisation
of both ventricles, approximately 0.2 seconds after the initial impulse has arisen in the
sinoatrial node. Depolarisation of the myocardial cell membrane causes a large increase
in the concentration of calcium within the cell, which in turn causes contraction by a
temporary binding between two proteins, actin and myosin. The cardiac action potential
is much longer than that of skeletal muscle, and during this time the myocardial cell is
unresponsive to further excitation.

The electrical activity of the heart

Autorhythmicity- beats on its own

99% heart contractile muscle cells

1% autorhythmic cells- specialise for initiating & conducting the action potentials

Action Potential:
Membrane potential slowly depolarises between action potentials until threshold is
reached & action potential fired

Resting potential cardiac muscle fibres - 90 mv

This is due to the movement of ions less K+ leaves the cell because it becomes less
permeable to K+

but Na+ can still enter

So inside of cell becomes less negative up to threshold value

At threshold-
1. Na+ channels open rapidly, Na+ rush into the cell

2. Voltage gated slow Ca++ channels open in plasma membrane and membrane of
sarcoplasmic reticulum allowing Ca++ to enter the cell producing the rising phase of the
action potential. Modulation of activity Ca++ channels → alters force contraction

Combination of 1+2 maintains depolarisation for 250 msec → plateau on graph (skeletal
muscle action potential 1 msec)

As the action potential increases it causes voltage gated K+ channels to open and K+ can
leave the cell

The membrane potential falls as K+ leaves and this causes the K+ channels to shut

Refractory period - period when heart not responsive to stimulation absolute and

Prevents the heart from seizing up

Autorhythmic cells:-

Sinoatrial node (pacemaker i.e. starts here) 70-80 beats/min

Atrioventricular node 40-60 beats/min

Atrioventricular bundle (Bundle of His) 20-40 beats/min
Pukinje Fibres 20-40 beats/min

SAN fastest-drives the rest

Action potential in cardiac muscle is due to movement of Na+ in & K+ out

but lasts longer than other muscle types because Ca++ moves in slowly so tetanus

The spread of cardiac excitation is co-ordinated to assure efficient pumping

Atrial excitation and contraction should be complete before onset of ventricular

contraction (AV nodal delay-0.1second)

Excitation of cardiac muscle should be co-ordinated so that each heart chamber contracts
as a unit to accomplish efficient emptying

The pair of atria and pair of ventricles should be functionally co-ordinated so that both
members of the pair contract simultaneously

The cardiac cycle

The relationship between electrical and

mechanical events in the cardiac cycle is
summarised in Figure 1.

There is a similar cycle on both sides of the

heart, but the pressures in the right ventricle
and pulmonary arteries are less than those in
the left ventricle and aorta.

Systole -2 phases
Diastole - 3 phases

Cardiac cycle alternate systole (contraction &

emptying) and diastole (relaxing &
filling).Systole refers to contraction, while
diastole refers to relaxation. Both contraction
and relaxation can be isometric, when changes
in intraventricular pressure occur without a
change in length of the muscle fibres. The
cycle starts with depolarisation at the

sinoatrial node leading to atrial contraction. Until this time blood flow into the ventricles
has been passive, but the atrial contraction increases filling by 20-30%Ventricular systole
causes closure of the atrioventricular valves (1st heart sound), and contraction is
isometric until intraventricular pressures are sufficient to open the pulmonary and aortic
valves, when the ejection phase begins.

The volume of blood ejected is known as the stroke volume. At the end of this phase
ventricular relaxation occurs, and the pulmonary and aortic valves close (2nd heart
sound). After isometric relaxation ventricular pressures fall to less than atrial pressures.
This leads to opening of the atrioventricular valves and the start of ventricular diastolic
filling. The whole cycle then repeats following another impulse from the sinoatrial node.

The coronary circulation

Myocardial blood supply is from the right and left coronary arteries, which run over the
surface of the heart giving branches to the endocardium (the inner layer of the
myocardium). Venous drainage is mostly via the coronary sinus into the right atrium, but
a small proportion of blood flows directly into the ventricles through the Thebesian veins,
delivering unoxygenated blood to the systemic circulation. Oxygen extraction by the
tissues is dependent on consumption and delivery. Myocardial oxygen consumption is
higher than in skeletal muscle (65% of arterial oxygen is extracted as compared to 25%).
Therefore any increased myocardial metabolic demand must be matched by increased
coronary blood flow. This is a local response, mediated by changes in coronary arterial
tone, with only a small input from the autonomic nervous system.

Cardiac Output

Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV):

CO = HR x SV

For a 70kg man normal values are HR=70/min and SV=70ml, giving a cardiac output of
about 5litre/min. The cardiac index is the cardiac output per square metre of body surface
area - normal values range from 2.5-4.0 litre/min/m2.
Heart rate is determined by the rate of spontaneous depolarisation at the sinoatrial node
(see above), but can be modified by the autonomic nervous system. The vagus nerve acts
on muscarinic receptors to slow the heart, whereas the cardiac sympathetic fibres
stimulate beta-adrenergic receptors and increase heart rate.

Stroke volume is determined by three main factors: preload, afterload and contractility.
These will be considered in turn:

Preload is the ventricular volume at the end of diastole. An increased preload leads to an
increased stroke volume. Preload is mainly dependent on the return of venous blood from
the body. Venous return is influenced by changes in position, intra-thoracic pressure,
blood volume and the balance of constriction and dilatation (tone) in the venous system.
The relationship between ventricular end-diastolic volume and stroke volume is known as
Starling's law of the heart, which states that the energy of contraction of the muscle is
related/proportional to the initial length of the muscle fibre. This is graphically illustrated
in Figure 2 by a series of "Starling curves".

Curves A and B illustrate the rise in cardiac output

with increases in ventricular end-diastolic volume
(pre-load) in the normal heart. Note that with an
increase in contractility there is a greater cardiac
output for the same ventricular end- diastolic volume.

In the diseased heart (C and D), cardiac output is

leass and falls if ventricular end-diastolic volume
rises to high levels, as in heart failure or overload.

As volume at the end of diastole (end-diastolic volume) increases and stretches the
muscle fibre, so the energy of contraction and stroke volume increase, until a point of
over-stretching when stroke volume may actually decrease, as in the failing heart.
Cardiac output will also increase or decrease in parallel with stroke volume if there is no
change in heart rate.

The curves show how the heart performs at different states of contractility, ranging from
the normal heart to one in cardiogenic shock. This is a condition where the heart is so
damaged by disease that cardiac output is unable to maintain tissue perfusion. Also
shown are increasing levels of physical activity which require a corresponding increase in
cardiac output.

Afterload is the resistance to ventricular ejection. This is caused by the resistance to flow
in the systemic circulation and is the systemic vascular resistance. The resistance is
determined by the diameter of the arterioles and pre-capillary sphincters; the narrower or
more constricted, the higher the resistance. The level of systemic vascular resistance is
controlled by the sympathetic system which, in turn, controls the tone of the muscle in
the wall of the arteriole, and hence the diameter. The resistance is measured in units of
dyne.sec/cm5. A series of Starling curves with differing afterloads is shown in Figure 3,
demonstrating a fall in stroke volume as afterload increases.

The relationship between stroke volume and
afterload. A series of curves illustrates the effects of
increasing afterload on systemic vascular resistance.
As afterload increases, the patient moves to a lower
curve, with a lower stroke volume for the same
ventricular end-diastolic volume (preload).

The relationship between systemic vascular

resistance and the control of arterial pressure is
discussed below.

Contractility describes the ability of the myocardium to contract in the absence of any
changes in preload or afterload. In other words, it is the "power" of the cardiac muscle.
The most important influence on contractility is the sympathetic nervous system. Beta-
adrenergic receptors are stimulated by noradrenaline released from nerve endings, and
contractility increases. A similar effect is seen with circulating adrenaline and drugs such
as ephedrine, digoxin and calcium. Contractility is reduced by acidosis, myocardial
ischaemia, and the use of beta-blocking and anti-arrhythmic agents.

Cardiac output will change to match changing metabolic demands of the body. The
outputs of both ventricles must be identical, and also equal the venous return of blood
from the body. The balancing of cardiac output and venous return is illustrated during the
response to exercise. Blood vessels dilate in exercising muscle groups because of
increased metabolism, and blood flow increases. This increases venous return and right
ventricular preload. Consequently more blood is delivered to the left ventricle and cardiac
output increases. There will also be increased contractility and heart rate from the
sympathetic activity associated with exercise, further increasing cardiac output to meet
requirements. tissue

The systemic circulation

The systemic blood vessels are divided into arteries, arterioles, capillaries and veins.
Arteries supply blood to the organs at high pressure, whereas arterioles are smaller
vessels with muscular walls which allow direct control of flow through each capillary
bed. Capillaries consist of a single layer of endothelial cells, and the thin walls allow
exchange of nutrients between blood and tissue. Veins return blood from the capillary
beds to the heart, and contain 70% of the circulating blood volume, in contrast to the 15%
in the arterial system. Veins act a reservoir, and venous tone is important in maintaining
the return of blood to the heart, for example in severe haemorrhage, when sympathetic
stimulation causes venoconstriction.

Blood flow

The relationship between flow and driving pressure is given by the Hagen-Poisseuille
formula. This states that flow rate in a tube is proportional to:

Driving pressure x Radius4

Length x Viscosity
In blood vessels flow is pulsatile rather than continuous, and viscosity varies with flow
rate, so the formula is not strictly applicable, but it illustrates an important point; small
changes in radius result in large changes in flow rate. In both arterioles and capillaries
changes in flow rate are brought about by changes in tone and therefore vessel radius.

Viscosity describes the tendency of a fluid to resist flow. At low flow rates the red blood
cells stick together, increasing viscosity, and remain in the centre of the vessel. The blood
closest to the vessel wall (which supplies side branches) therefore has a lower
haematocrit. This process is known as plasma skimming. Viscosity is reduced in the
presence of anaemia, and the resulting increased flow rate helps maintain oxygen

delivery to the tissues.

Control of the systemic circulation

Autonomic control is largely by the sympathetic nervous system, which supplies all
vessels except capillaries. Sympathetic fibres arise from the thoracic and lumbar
segments of the spinal cord. These are under the control of the vasomotor centre in the
medulla, which has distinct vasoconstrictor and vasodilator areas.

Although there is a baseline sympathetic discharge to

maintain vascular tone, increased stimulation affects
some organs more than others (Figure 4). This tends
to redistribute blood from skin, muscle and gut to
brain, heart and kidney. Increased sympathetic
discharge is one of the responses to hypovolaemia,
for example in severe blood loss, with the effect of
protecting blood supply to the vital organs. The
predominant sympathetic influence is
vasoconstriction via alpha-adrenergic receptors.
However, the sympathetic system also causes
vasodilation via beta adrenergic and cholinergic
receptor stimulation, but only in skeletal muscle.

Circulating hormones such as adrenaline and angiotensin II are potent vasoconstrictors,

but they probably have little effect on acute cardiovascular control. In contrast,
endothelium derived factors play an important role in controlling local blood flow. These
substances are either produced or modified in the vascular endothelium, and include
prostacyclin and nitric oxide, both potent vasodilators. An accumulation of metabolites
such as CO2, K+, H+, adenosine and lactate causes vasodilation. This response is probably
an important mechanism of autoregulation, the process whereby blood flow through an
organ is controlled locally, and remains constant over a wide range of perfusion pressure.
Autoregulation is a particular feature of the cerebral and renal circulations.

Control of arterial pressure

Systemic arterial pressure is controlled closely in order to maintain tissue perfusion. The
mean arterial pressure (MAP) takes account of pulsatile blood flow in the arteries, and is
the best measure of perfusion pressure to an organ. MAP is defined:

MAP = Diastolic arterial pressure + (pulse pressure / 3)

where pulse pressure is the difference between systolic and diastolic arterial pressure.

MAP is the product of cardiac output (CO) and systemic vascular resistance (SVR):


If cardiac output falls, for example when venous return decreases in hypovolaemia, MAP
will also fall unless there is a compensatory rise in SVR by vasoconstriction of the
arterioles. This response is mediated by baroreceptors, which are specialised sensors of
pressure located in the carotid sinus and aortic arch, and connected to the vasomotor
centre. A fall in blood pressure causes reduced stimulation of the baroreceptors, and
consequent reduced discharge from the baroreceptors to the vasomotor centre. This
causes an increase in sympathetic discharge leading to vasoconstriction, increased heart
rate and contractility, and secretion of adrenaline. Conversely, rises in blood pressure
stimulate the baroreceptors, which leads to increased parasympathetic outflow to the
heart via branches of the vagus nerve, causing slowing of the heart. There is also reduced
sympathetic stimulation to the peripheral vessels causing vasodilation.

Baroreceptor responses provide immediate control of blood pressure; if hypotension is

prolonged, other mechanisms start to operate, such as the release of angiotensin II and
aldosterone from the kidneys and adrenal glands, which leads to salt and water being
retained in the circulation.


Noninvasive procedures provide important information in addition to that provided by the

history and physical examination. Invasive procedures may also be needed


Although left ventricular wall thickness and mass tend to increase with age, no age-
specific criteria for ECG diagnosis of left ventricular hypertrophy have been developed.
Limb lead and precordial QRS voltages decrease with age. Age-related increases in the
frequency of ectopic beats, in PR and QT intervals, in left axis deviation, and in the
frequency of right bundle branch block have no prognostic significance for elderly
persons without clinical evidence of heart disease.The most common ECG abnormality in
the elderly is nonspecific changes in ST segments or T waves, which are often due to use
of digoxin, a diuretic, an antiarrhythmic, or a psychoactive drug; such changes have little
independent prognostic significance. However, if the patient is not using any of these
drugs and if voltage criteria for left ventricular hypertrophy are met, these changes
predict an increased risk of cardiovascular morbidity and mortality.

In the elderly, an ECG pattern of poor R-wave progression in leads V 1 to V4 has low
specificity and predictive value for anterior myocardial infarction (MI), probably because
of age-related increases in resting lung volume and anteroposterior chest diameter. Thus,
ECG may not be as useful in detecting silent MI in the elderly as in younger persons.

Ambulatory ECG monitoring, usually for 24 hours, is useful for elderly patients with
unexplained syncope, palpitations, or other evidence suggesting major arrhythmias or
conduction disorders. Patients with known organic heart disease, especially those who
have had an MI, are appropriate candidates because they are the most likely to have a
major arrhythmia during monitoring. However, because complex arrhythmias during
ambulatory ECG monitoring are relatively common among healthy elderly persons,
patients should record symptoms in a diary so that symptoms can be correlated with ECG
rhythm disturbances. Ambulatory ECG monitoring is also useful for detecting
asymptomatic episodes of myocardial ischemia.When symptoms are infrequent and
nondisabling, an ECG event recorder is a better choice because it is economical and can
provide up to 6 weeks of intermittent monitoring. Loop event recorders can capture up to
4 minutes of retrospective ECG data before patient activation and can transmit the ECG
via telephone to a central recording facility when symptoms occur.

Electrophysiologic Testing

Electrophysiologic testing includes recording of His bundle activity, atrial pacing,

programmed atrial or ventricular stimulation, and mapping of tachyarrhythmias.
However, in elderly patients, it is used mainly for programmed ventricular stimulation
when coronary artery disease (CAD) or a life-threatening ventricular arrhythmia is
present. Electrophysiologic testing in the elderly has a low morbidity rate and helps
determine the need for antiarrhythmic drugs or for an implantable cardioverter-

Table Tilt Testing

Tilt table testing is usually recommended for patients who have unexplained syncope but
do not have structural heart disease. Patients are typically tilted at a 60 to 80° angle on a
motorized table for 15 to 20 minutes while their blood pressure and heart rate are
continuously monitored. If hypotension (with or without bradycardia) does not occur,
patients are given an infusion of isoproterenol sufficient to accelerate the heart rate by 20
beats/minute, and the test is repeated. The procedure produces many false-positive results
and must be used only for patients with definite syncope and negative ambulatory ECG
results. Diagnostic sensitivity tends to be lower but specificity tends to be higher in
elderly patients with syncope than in younger patients.

Exercise Testing

Exercise testing is generally safe for the elderly Treadmill or bicycle exercise testing
with continuous ECG monitoring is an efficient, inexpensive procedure for diagnosing
CAD and determining the prognosis for patients with known CAD, especially those who
have had an MI. Test sensitivity increases with patient age, from 56% in patients < 40 to
85% in those > 60. This correlation is consistent with the higher prevalence and greater
severity of CAD in the elderly. Test specificity decreases modestly with patient age, from
84% in patients < 40 to 70% in those > 60, probably because left ventricular hypertrophy,
nonspecific resting ST-segment abnormalities, and valvular heart disease are more
common among elderly patients.

Exercise-induced ST-segment depression has diagnostic and prognostic significance for

elderly patients with chest pain. A reduced exercise capacity, a blunted increase in the
heart rate-blood pressure product, and the occurrence of major ventricular arrhythmias
during exercise indicate high risk of cardiac death for elderly patients who have had an
MI.The following age-related changes should be considered when exercise testing is
performed in elderly patients:

• The elderly have a lower maximal aerobic capacity, so testing should begin at a
level requiring low energy expenditure.
• Maximal heart rate decreases progressively by about 1 beat/ minute yearly until at
least about age 90.
• Systolic blood pressure at rest and at any given submaximal external workload is
higher in the elderly, although age-related differences are less prominent at
maximal effort.
• The ability to exercise is often limited by conditions unrelated to the heart (eg,
arthritis, neurologic disorders, peripheral vascular disease).
• Elderly persons may not exercise maximally because of psychologic factors (eg,
unfamiliarity with vigorous exercise, fear, insufficient motivation).

Alternatives to treadmill exercise testing include bicycle ergometry, arm ergometry, atrial
or esophageal pacing, and pharmacologic stress testing with IV dipyridamole, adenosine,
or graded IV infusions of dobutamine. If dobutamine increases the heart rate to < 85% of
predicted maximum, atropine may be added. These pharmacologic stress tests are safe
and effective for elderly patients and are preferred when patients cannot perform
treadmill or bicycle exercise--eg, because of musculoskeletal or pulmonary disorders.

Thallium-201 myocardial perfusion scintigraphy during exercise or pharmacologic stress

testing is considered the most accurate noninvasive test for detecting CAD in all age
groups. Perfusion defects detected at rest generally indicate a previous MI. Segmental
defects that are detected during exercise (or pharmacologic stress testing) and that resolve
or improve within 3 to 4 hours indicate exercise-induced ischemia. This imaging
procedure can be used to screen for CAD in the many elderly patients who have left
ventricular hypertrophy or bundle branch block or who are receiving digoxin or other
antiarrhythmic drugs.

The procedure's sensitivity and specificity for CAD is nearly 90% for patients of all ages.
The extent of the exercise-induced defect is a useful prognostic indicator for elderly
patients with known or suspected CAD. Adding tomographic imaging increases
sensitivity but may decrease specificity for mild disease. In patients >= 70, IV
dipyridamole-thallium imaging has a sensitivity of 86% and a specificity of 75%. Use of
IV adenosine instead of dipyridamole results in a higher incidence of adverse effects,
such as conduction system disturbances or arrhythmias caused by impulse formation.

Technetium-99m sestamibi produces better images than thallium and is useful for elderly
patients with chronic obstructive pulmonary disease or marked obesity.

Chest X-ray

When rales are detected, a chest x-ray may be indicated to document left-sided heart
failure. When pulmonary hypertension is suspected, a chest x-ray can confirm the
diagnosis by showing large central pulmonary arteries with oligemic lung fields.

Aortic knob calcification is detected in about 30% of the elderly but has no pathologic
significance. In contrast, intracardiac calcification, most commonly on the aortic valve
and the mitral annulus, is almost always pathologic; it signifies valvular stenosis. In the
elderly, coronary artery calcification, best seen with fluoroscopy, does not necessarily
signify major stenosis, as it does in younger patients. Calcification of the pericardium
(due to constrictive pericarditis) or the left ventricular wall (due to an old MI) is
occasionally also seen.


In the elderly, echocardiography is useful for assessing left ventricular chamber size and
function after diagnosis of heart failure or after acute MI; for assisting in the differential
diagnosis of systolic murmurs, especially those grade 3/6 or higher in loudness; for
measuring left atrial size and assessing left ventricular function in patients with new atrial
fibrillation; for determining pulmonary artery pressures in patients with heart failure; for
confirming the presence of pericardial effusion or tamponade; and for detecting a left
ventricular aneurysm. Echocardiography can detect thickened aortic or mitral valve
leaflets or a calcified mitral annulus, which are the most common sources of systolic
murmurs in the elderly. Atrial myxomas, left ventricular thrombi, and valvular
vegetations are best detected by echocardiography.

Echocardiography performed immediately after treadmill or pharmacologic stress testing

may be used instead of radionuclide perfusion imaging to detect myocardial ischemia
(which is indicated by wall motion abnormalities) and to determine prognosis. For
patients >= 70, dobutamine stress echocardiography, which is the preferred noninvasive
test for the elderly by many clinicians, has a sensitivity of 87%, a specificity of 84%, and
an accuracy of 86% for the diagnosis of CAD. Adenosine stress echocardiography has a
sensitivity of 66%, a specificity of 90%, and an accuracy of 73%. Exercise
echocardiography has a sensitivity of 85% and a specificity of 77%.

M-mode echocardiography can detect age-related changes such as small increases in

aortic root and left atrial dimensions, an increase in left ventricular wall thickness with no
change in cavity size, and a decrease in mitral valve E-F closure slope (the rate of mitral
valve closure in early diastole). Despite these changes, values for elderly persons usually
remain within the limits of what is considered normal for younger persons.

Doppler echocardiography is used to quantify aortic valve stenosis. It is also used to

assess diastolic dysfunction, particularly in patients with heart failure of unclear etiology.
Doppler echocardiography can be used to predict length of survival for elderly patients
with heart failure on the basis of E- and A-wave velocity measurements. Color Doppler
echocardiography, with flow mapping, is useful for detecting and estimating the severity
of valvular regurgitation. Mild multivalvular regurgitation is common among otherwise
healthy elderly persons, so regurgitation is significant only if it is moderate or severe.

Transesophageal echocardiography is safe for elderly patients and should be considered

for those with suspected heart disease if transthoracic echocardiography is not diagnostic.
Transesophageal echocardiography is particularly useful for detecting aortic dissection,
valvular vegetations, thrombi in the left atrium or left atrial appendage, and prosthetic
valve dysfunction in patients who have the appropriate clinical presentation. Elderly
patients with intra-aortic atherosclerotic debris detected by transesophageal
echocardiography are at increased risk of thromboembolic events during cardiac surgery.

Intravascular ultrasonography allows detailed morphologic assessment of CAD but is

expensive and invasive. This procedure may be useful for determining the suitability of a
specific intervention (eg, balloon angioplasty, laser therapy, stent placement) for patients
with CAD.

Radionuclide Ventriculography
Radionuclide ventriculography is the most accurate procedure for assessing global left
and right ventricular function. It is especially useful for patients with chest wall
abnormalities or pulmonary hyperinflation (about 25% of elderly patients), because
technically adequate echocardiograms cannot be obtained in them. Two techniques are
used: With the first-pass technique, the initial passage of technetium 99m through the
cardiac chambers is recorded. With the more commonly used gated blood pool
(equilibrium) technique, technetium 99m is allowed to equilibrate in the blood, and then
ECG-gated (synchronized) images are recorded during many cardiac cycles. Both
techniques can accurately measure global and regional left ventricular systolic
performance as well as changes in left ventricular volume.

In elderly patients with suspected CAD, the first-pass or gated technique can be used to
measure the left ventricular ejection fraction during bicycle exercise. Radionuclide
ventriculography (as well as myocardial perfusion imaging) is particularly useful when
ST-segment changes cannot be reliably interpreted because of left bundle branch block,
left ventricular hypertrophy, or treatment with digoxin. An abnormal exercise response in
elderly persons is best defined as any decrease in ejection fraction from the resting value.
A regional wall motion abnormality that occurs during exercise is considered a specific
indicator of CAD.

Positron Emission Tomography

Positron emission tomography is used to assess myocardial blood flow and metabolism.
The procedure is very sensitive, but its diagnostic usefulness in the elderly is unknown. It
is costly and requires an on-site cyclotron to generate radioisotopes.

Computed Tomography

CT of the heart is useful for diagnosing cardiac masses and pericardial effusions and may
help detect pericardial thickening and distinguish pericardial fat from effusion. Echo-free
pericardial spaces, indicating fat or effusion, increase in prevalence with age and occur in
about 10% of women > 80.

Electron-beam CT detects CAD by determining the density of calcifications in the arterial

wall; a calcium score above a predetermined threshold suggests significant luminal
narrowing. The presence of calcium in coronary arteries is highly specific for CAD in
younger patients; however, with age, this specificity decreases, from 74% in patients < 40
to 34% in those > 50. Because of the low specificity, this procedure is not recommended
for diagnosing CAD in the elderly. The patency of coronary artery bypass grafts can be
assessed using this procedure. It may be used instead of cardiac catheterization after
bypass surgery, but IV injection of iodinated contrast media is required.

Magnetic Resonance Imaging

MRI can characterize cardiac anatomy and metabolism without use of ionizing radiation.
It can assess myocardial viability in patients who have had an infarction and in those who
have chronic heart failure or many other disorders. It is an alternative to
echocardiography for measuring chamber size and thickness. ECG-gated imaging allows
ventricular function assessment; however, it is expensive, restricting its use in primary

Cardiac Catheterization and Coronary Angiography

Cardiac catheterization with coronary angiography remains the gold standard for
diagnosis and quantitation of CAD. It is the only procedure that directly measures
intracardiac pressures and defines coronary artery anatomy. The risks of cardiac
catheterization, including cerebral and peripheral embolization, renal failure, and death,
are increased for the elderly. Risks may be increased because elderly patients are more
likely to have preexisting coronary and peripheral vascular disease, renal insufficiency,
and left ventricular dysfunction.The incidence of death and major complications
associated with coronary angiography in patients >= 60 is low but is still significantly
higher than that in younger patients . The incidence is higher in the elderly partly because
cardiomegaly and left ventricular dysfunction are more common and because obtaining
vascular access is more difficult. Nonetheless, coronary angiography is appropriate for
elderly patients with CAD when revascularization is being considered.Digital subtraction
angiography, a computer-enhanced imaging technique, may be safer because the amount
of contrast media can be reduced by 75%.

Heart disease is any disorder that affects the heart’s ability to function normally. The most
common type of heart disease is coronary artery disease, which is the narrowing or
blockage of the coronary arteries. Some people are born with abnormalities (congenital
heart disease). Various forms of heart disease include:

• Coronary artery disease (the most common form of heart disease)

• Arrhythmias (abnormal heart rhythms)
• Heart failure
• Heart valve diseases
• Congenital heart disease

Risk Factors

There are many risk factors for heart disease; some are inherited, but others are quite

Uncontrollable risk factors include:

• Family history of heart disease (especially with onset before age 55)
• Diabetes mellitus
• Age (65 and older)
• Women, after the onset of menopause — generally men are at risk at an earlier
age than women, but after menopause, women are equally at risk

Controllable risk factors:

• Cigarette smoking
• Being overweight by 30 percent
• Hypertension -- high blood pressure
• High cholesterol levels (specifically, high LDL cholesterol and low HDL
cholesterol and high triglycerides)
• Stressful lifestyle
• Sedentary lifestyle (physical inactivity)


Treatment of cardiovascular disease are various types of durgs are present to prevation
and cure the heart disease it is clsiified following types

• Digoxin

• Propranolol
• Propranolol with Alprazolam
• Propranolol with Diazepam
• Metoprolol
• Atenolol
• Atenolol with Alprazolam
• Atenolol with Indapamide
• Atenolol with Asprin
• Labetalol
• Bisoprolol
• Esmolol Hydrochloride
• Carvidilol
• Nebivolol
• Phentolamine Mesylate

Membrane Stabilizing Agents:
• Quinidine
• Procainamide
• Lidocaine (Lignocaine)
• Mexiletine
• Adenosine
Agents Widening AP (Prolong Repolarization)
• Amiodarone
Calcium Channel Blockers
• Verapamil
Sympathetic Inhibitors:
• Clonidine
• Reserpine
• Prazocine
• Hydralazine/Dihydralazine
• Indapamide
• Terazocine
• Doxazocin
• Lacidipine
• Lercanidipine
ACE Inhibitors:
• Captopril
• Enalapril Maleate
• Lisinopril
• Perindopril
• Ramipril
• Ramipril with Metopralol
• Benazepril
• Trandolapril
• Fosinopril
• Imidapril
• Losartan Potassium
• Losartan Potassium With Ramipril
• Losartan Potassium with Amlodipine
• Losartan potassium with Enalapril maleate
• Irbesartan
• Candesartan
• Valsartan
• Amrinon
• Milrinone
• Phenoxybenzamine

• Frusemide
• Torasemide
• Spironolactone
• Triamterene and Amiloride
• Hydrochlorothiazide
• Chlorthalidone
• Acetazolamide
• Xipamide
• Telmisartan
• Glyceryl Trinitrate (GTN, NITROGLYCRINE)
• Nicorandil
• Isosorbide Dinitrate
• Isosorbide 5 Mononitrate
• Nifedipine
• Nifedipine and Atenolol
• Benidipine HCL
• Verapamil
• Diltiazem
• Felodipine
• Atenolol and Nitrendipine
• Amlodipine
• Amlodipine with Atenolol
• Amlodipine with Enalapril
• Amlodipine with Lisinopril
• Amlodipine with Ramipril
• Amlodipine with Benazepril
• Amlodipine with Atorvastatin
• S(-) Amlodipine
• Dilazep
• Oxyfedrine
• Trimetazidine

• Isoxsuprine, Nylidrine
• Ginkgo Biloba
• Cinnarizine
• Cyclandelate
• Xanthinol Nicotinate
• Pentoxifylline

• Vitamine K
• Ethamsylate
• Tranexamic Acid
• Calcium Dobesilate
• Cardioplegia
• Polidocanal
• Sodium Tetradecyl

• Adrenochrome Monosemicarbazone
• Apotinin
• Rutin
• Flavonoids
• Diosmin
• Protamine Sulphate

• Heparine
• Reviparine Sodium
• Enoxaparin
• Nadroperin
• Coumarins & Indanediones
• Tissue Type Plasminogen Activator
• Streptokinase
• Urokinase
• Abciximab
• Warfarin

• Asprine
• Clopidogrel
• Cilostazole
• Ticlopidine

• Dopamine HCL
• Dobutamine Hydrochloride
• Mephentermine
• Phenylephrine


DIGOXIN: It has direct effects on myocardial contractility and

electrophysiological conduction properties i.e. Negative chronotropic effects and
positive inotropic effect.

Dosages: Initially 0.25-1.5mg daily and 0.25-0.5mg daily children, initially 10-
20 mcg/kg body wt. Hrly. Maint 10-20 mcg/kg body wt. In single or divided
doses daily.
1. Lanoxin (Digitoxin) GSk(Glaxo smithkline)

Tab. 0.25mg 10x1 9.98

2. Cardioxin Novartis India

Tab. 0.25mg 10x1 5.00
Inj. 0.05mg/2ml 10ml 19.25

3. Digitran Macleods
Tab. 0.25mg 10x1 5.85

4. Digoxin Burroughs wellcome

Ped. Elixer 30mlx1 21.03
Inj. 05mg/2ml 2mlx1 5.31



Category- Beta blockers, Antihypertensive

Action : A non selective beta blockers. Heart rate and cardiac output and
reduced. Initially peripheral resistance may be increased but in long term it
returns to pretreatment levels. Blood pressure is reduced as is myocardial
work load. In anginal patients exercise tolerance is increased are attacks
reduced. Propranolol exerts a quinidine like membrane stabilizing action and
is useful in cardiac arrhythmias.

Dosage: 10 mg BD to 160mg QID (avg. 40-160mg/day)

1. Betabloc (Propranolol Hcl) U.S.V.

Tab. 10mg 10x1 3.00

2.Ciplar Cipla
Tab 10mg 10x1 7.75
40mg 10x1 17.75

3. Betacap T.R. Natco

Cap. 40mg 10x1 19.90
80mg 10x1 30.50

4. Inderal ICI
Tab. 10mg 10x1 7.88
40mg 10x1 19.98
80mg 10x1 29.89

Category: Cardio selective Beta blockers, Antihypertensive
Action: Inhibite of Beta-1 receptors by metoprolol results in reduced heart
rate and lowered blood pressure, Cardiac output is reduced. Renin release is
inhibited. Less potential for -bronchoconstriction.

Dosage: Adults- 100-20mg in two divided doses.

Children- 1-5mg/kg/day in two divied doses.

1. Betaloc (Metoprolol) Astra Zeneca

Tab. 25mg. 1x10mg 14.52
50mg 1x10mg 21.53
100mg 1x10mg 33.73
Inj. 1ml/mg 3x5ml 39.00

2. Metolar Cipla
Tab. 25mg 1x10mg 12.75
50mg 1x10mg 20.75
100mg 1x10mg 31.25
Inj. 1mg/ml 5ml 7.75
Metolar XR (Metoprolol Extended rease) Cipla
Cap. 50mg 1x10 44.25
100mg 1x10 62.25

3. Lopresor (Metoprolol tartrate) Novartis

Tab. 50mg 1x10 24.50
100mg 1x10 42.50


Category: Beta blockers, Antihypertensive

Action: It is a relatively cardio selective beta andrenoceptor blocking
agent without membrane stabilizing or intrinsic sympathomimetic activities.
Following oral doses of 50 or 100 mg. Both beta blocking and antihypertensive
effects persists for at least 24hrs. because of higher lipid solubility.

Dosage: Adults- 50-100mg daily

Children- 1-1.3mg/kg/day daily or two divided doses.

1. Atpark (Atenolol) Parke-Davis

Tab. 25mg 1x14 15.75
50mg 1x14 23.50
100mg 1x14 38.42

2. Tenolol Ipca
Tab. 25mg 1x14 17.85
50mg 1x14 25.75
100mg 1x14 41.50

3. Betacard Torrent
Tab. 25mg 1x14 19.24
50mg 1x14 28.06
100mg 1x14 47.71

4. Tenormin Nicolas Piramal

Tab. 25mg 1x14 20.50
50mg 1x14 25.75
100mg 1x14 41.50

5. Atekind Mankind
Tab. 50mg 1x14 7.70

6. Atecard Dabur
Tab. 25mg 1x14 12.00
50mg 1x14 23.30
100mg 1x14 35.00

7. Tenormin Nicholas Piramal

Tab. 25mg 1x14 20.50
50mg 1x14 31.00
100mg 1x14 52.58


Category: Beta blockers, Antihypertensive.

Action : It is a competitive antagonist of the beta-adrenergic receptors. It has high
beta selectivity. There is no membrane stabilising or partial agonist action.
Reduction in heart rate and blood pressure. Action lasts for 24hrs.

Dosage: Start at 2.5 or 5mg/day and build up to 10-20mg/day. Dose

reduction in severe renal impairment.

1. Concor (Bisoprolol) Merck

Tab. 5mg 1x10 40.12

2. Corbis (Unisearch) Neu-foreva

Tab. 2.5mg 1x10 15.00
5mg 1x10 17.50
10mg 1x10 30.00

Category: Beta bolockers, Antihypertensive
Action : It is an arylethanolamine non specific beta adrenoreceprtor anatagonist
with alpha-1 blocking activity. It exerts antihypertensive effect partly by reducing
total peripheral resistance and vasodilation by blocking alpha-1 adrenoreceptors
and by inhibition beta adrenoreceptor mediated compensatory mechanisms.

Dosage: Hypertension- initially 6.25mg twice daily. If tolerated after 7-14 days,
increases to 12.5mg twice daily if needed. If needed again increase the dose up to
25mg twice daily,after 7-14 days. Max total daily dose 50mg.
Congestive heart failure: Start with 3.125mg twice daily for 2weeks. If
tolerated, raise to 6.25mg twice daily and then double the dose every 2 weeks th
the level tolerated by patients weighing less than 85kgs and more than 85kgs

1. Cardivas (Carvedilol) Sun Pharma

Tab. 3.125mg 1x10 11.00
6.25mg 1x10 19.00
12.5mg 1x10 42.00
25mg 1x10 73.00

2. Carvas Medley(Vazokare)
Tab. 3.125mg 1x10 9.00
6.25mg 1x10 16.00
12.5mg 1x10 29.00
25mg 1x10 55.00

3. Carvil Zudus cadila

Tab. 3.125mg 1x10 14.50
6.25mg 1x10 21.00
12.5mg 1x10 31.80


Category: Local anaesthetic
Action : It is a local anaesthetic which stabilizes the neuronal membrane and
inhibits the ion movements which are necessary for conduction of impulses. In the
heart lignocain reduces phase 4 depolarisation, decreases automatically. Duration
of action potential and effective refactory period is reduced.

Dosage: 1mg/kg body wt. By slow i.v. bolus over a period of 5-10 mts. With same
or reduced dosage.

1. Xylocaine Astra Zeneca
Sol. 2% 100ml 16.61
Oint. 5% 20gm 20.91
Jelly 2% 30gm 27.19

2. Xylocain Heavy 5% Astra Zeneca

Inj. 2ml 25x2ml 101.00

3. Gesicard (anhydrous lignocain) Nicholas piramal

Inj. 20mg/ml 1x5ml 1.07
1x50ml 9.06

Category: Antiarrhythmic
Action : It is a long acting, prominent action being prolongation of APD and ERP
in atria, A-V node ,conducting tissue and ventricular fibres.

Dosage: 200mg thrice daily for once week than 200mg twice daily for one week.
Maintain on minimum effective dose: 200mg daily.

1.Cordarone (amiodaron Hcl) Torrent

Tab. 100mg 1x10 55.12
Inj. 1x3ml 56.53
Tab. 200mg 1x10 107.40

2. Aldarone Alidac cadila

Inj. 50mg/ml 1x3ml 11.30


Category: Antihypertensives, Antianginal and Coronary, Vasodilators,
Action : Verapamil inhibit entry of calcium ions into arterial smooth muscles cells
as well as myocytes and conducting tissue. These action lead to reversal and
preventions coronary artery spasm, reduction in after load through peripheral
vasodilatation and reduction in ventricular rate in patients with chronic atrial
flutter or fibrillation and reduction the occurrence of paroxysmal supravantricular
tachycardia. Verapamil reduces bloods pressure, relives angina and controls

Dosage: Adults- Oral 40-80mg 3-4 times a day. Max 480mg dailyn.
Children- Oral less than 6 yrs. Upto 40mg BD or Tid. 6-12 yrs. 40-120mg BD or
Tid. Max. 360mg/day.

1. Calaptin Nicholas piramal
Tab. 40mg 1x10 6.85
80mg 1x10 12.77
SR 120mg 1x10 21.72
240mg 1x10 41.47

2. Vasopten Torrent
Tab. 40mg 1x10 8.86
80mg 1x10 17.38
120mg 1x10 14.03

Category : Antihypertensive, antiarrhythmic.
Action : Diltiazem blocks the ‘L’ type calcium channels which are present in
heart and blood vessels. It reduces heart rate and blood pressure in a parallel way.
There is no reflex tachycardia. Peripheral arteries are dilated, resistance and after
lode reduced. Coronary vessels are dilated and there is improvement in collateral
circulation. Spontaneous coronary spasm is prevented. Diltiazem converts
paroxymal supraventricular tachycardia to normal sinus rhythm.

Dosage: Initially 30mg, 2-4 times daily before meals and bed time, increase
gradually to max. 240mg 3-4 divided doses daily.

1. Dilcontin Modi Mundi

Tab. CR 60mg 10 60.30
XL 90mg 10 80.45
120mg 10 95.35
180mg 10 140.20

2. Dilzem Torrent
Tab. 30mg 10 21.05
60mg 10 40.09
SR 90mg 10 59.16
CD 120mg 10 80.19
180mg 10 110.26

3. Dilgard Protec
Tab. 30mg 10 21.25
60mg 10 32.54
XL 90mg 10 51.25
120mg 10 73.25
180mg 10 105.25

4. Angizem Sun pharma

Tab. 30mg 10 21.00
60mg 10 39.50
CD 90mg 10 57.50
CD 120mg 10 62.50
180mg 10 89.50

5. Onzem SR Novartis
Tab. 90mg 10 46.50
120mg 10 62.00

Category : Vasodilators, antianginal.
Action : It is potent vasodilator and atnianginal drug. Nifedipine causes
preferential dilation of coronary vessels and induces increase in coronary blood

Dosage: 5-20mg three times daily max. 120mg/day

1. Depin Zydus Cadila

Cap. 5mg 50x3 124.29
10mg 4x30 138.68
Retard 20mg 1x30 52.47

2. Depicor Merck
Cap. 5mg 1x10 8.62
10mg 1x10 10.32

3.Myogard RPG
Cap. 5mg 1x10 4.22


It is an alkaloid from the roots of Rauwolfia Serpentina (sarpgandha): It
produces slowly developing fall in BP and bradycardia. Taking 2-3 weeks for full
effects. The hypotensive is primarily due to depletion of N.A. from peripheral
adrenargic nerve ending.

Dosage: 0.25-0.5mg daily increased to 1-1.5mg if required injection ,

1-2mg i.m. once or twice daily till oral therapy is possible.

1. Adelphane Novartis
Tab. 0.1+10mg 10 6.90
Adelphane esidrex Novartis
Tab. 10 8.60

It is a selective competitive antagonist of the classical alpha 1 receptors. It
dilated resistance and capacitance vessels effects on the not appreciable impaired
by chronic therapy.

Dosage: Initially 0.5mg twice daily increasing to 1mg 2-3 times maint. 3-20 mg
daily inm divided doses.

1. Minipress XL Pfizer
Tab. 2.5mg 15 74.20
5mg 15 105.79
2. Prazopress Sun pharma
Tab. 1mg 10 21.75
2mg 10 40.50


Category : ACE inhibitors, Antihypertenssive.
Action : After de-esterification into the active enalapril, there is potent inhibition
of ACE, reduced levels of angiotensins II (AT II) and reduced aldosterone levels.
Clinically blood pressure is reduced, salt and water retention is corrected and
patients with congestive failure show considerable relief of symptoms.ventricular
hypertrohry is reversed. Renal blood flow is increased but in patients with renal
impairment there may be oliguria or acute renal failure.
Dosage: Essential and renovascular hypertension: initially 5mg once a day, if with
diuretic then 2.5mg maintain. Dose 10-20mg once daily. Maximum: 40mg once

1. Envas Cadila
Tab. 2.5mg 10 14.25
5mg 10 19.09
10mg 10 41.50

2. Nuril USVs
Tab. 2.5mg 10 13.00
5mg 10 21.00
10mg 10 38.60

3. Mayoce Merck
Tab. 2.5mg 10 12.00
5mg 10 17.50

4. Vasopril Protec
Tab 2.5mg 10 8.95
5mg 10 15.91

5. Enace Nicholas
Tab. 2.5mg 10 14.85
5mg 10 25.85
10mg 10 41.69
D 10 10.00

Category: Antihypertensives, Inotropic agents drugs and used in CHF.
Action: Competetive inhibition of ACE. Reduction in levels of angiotensin II and
aldosterone. Peripheral vasodilation and reduced peripheral resistance. BP
reduction Enhanced by salt and water depletion eg. Excessive sweating. In
patients with congestive failure, there is reduction in afterload and in pulmonary
capillary wedge pressure. Cardiac efficiency is increased as is also renal bllod

Dosage: Hypertension; Initially 10mg once daily maintain dose 20 40mg/day.

Maximum 80mg once daily. Congestive cardiac failure; initially 2.5mg once daily.
Maintain dose 5-20mg once daily.

1. Lipril (lisinopril) Lupin

Tab. 2.5mg 10 21.13
5mg 10 38.34
10mg 10 72.07

2. Biopril Biochem
Tab. 2.5mg 10 18.00
5mg 10 28.80
10mg 10 54.00

3. Zestril Nicholas
Tab. 2.5mg 7 21.00
5mg 7 38.00
10mg 7 70.00
20mg 7 133.00

Category: ACE inhibitor, Antihypertensive.
Action: A new long acting Ace inhibitor which is metabolized into the active
metabolite ramiprilat. High lipid solubility ensure good tissue peneitration
especially into the heart muscle and aortic wall. Has a higher affinity and more
persistent binding to ACE. In congestive failure pulmonary artery pressure and
pulmonary capillary wedge pressure are reduced. Cardiac function is improved.

Dosage: Hypertension: 2.5mg/day, maximum: 10mg/day. Cardiac failure:

1.25mg/day, increased to 2.5mg once daily, maximum : 10mg/day.

1. Cardace (ramipril) Sanofi Aventis

Tab. 1.25mg 10 30.75
2.5mg 10 56.84
5mg 10 97.02
10mg 10 134.10

2. Hopecard Aristo
Tab. 1.25mg 10 15.00
2.5mg 10 27.50
5mg 10 49.50
10mg 10 90.00

Category: ACE inhibitor, Antihypertensive.
Action : Benazepril and it’s metabolite benazeprilat inhibits angiotensin converting
enzyme, that catalyzes the conversion of angiotensin I to II. Angiotensin II also
stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results
in decreased plasma angiotensin II, which leads to decreased vasopressor activity
and to decreased aldosterone secretion.

Dosage: 10-40mg once daily.

1.Benace (Benazepril HCL) Novartis

Tab. 5mg 3x10 132.60
10mg 3x10 232.80

Category: Angiotesin II receptor antagonist, Antihypertensive
Action : Losartan is an angiotensin II receptor (type AT1) antagonist. Losartan
and its principle active metabolite block the vasoconstrictor and aldosterone-
seceting effects of angiotensin II by selectively blocking the binding of
angiotensin II to the AT1.

Dosage: 25-100mg once or twice daily. Starting and maintance dose: 50mg once
a day in volume depleted patients: 25mg once daily.

1. Alsertan (Losartan potassium) Aristo

Tab. 25mg 10 14.79
50mg 10 35.04
Alsertan H 10 40.00
(Losartan Potassium 50mg & Hydrochlorothiazide 12.5)

2. Tozaar Torrent
Tab. 25mg 10 23.05
50mg 10 48.61
Tozaar H 50+12.5mg 10 49.11

3. Losacar Zydus Cadila

Tab. 25mg 10 25.70
50mg 10 48.90
Losacar H 7 42.42

4. Losakind Mankind
Tab. 50mg 10 15.90
Losakind H 50+12.5mg 10 19.90
5. Zaart Cipla
Tab. 25mg 10 21.25
50mg 10 40.25
Zaart H 50+12.5mg 10 42.75
6. Losar Unisearch
Tab. 25mg 10 23.00
50mg 10 44.00
Losar H 50+12.5mg 10 49.00


1. Tozaar R Torrent
Tab. 2.5mg 10 59.14
5mg 10 69.66
2. Loram Unisearch
Tab. 50+1.25mg 10 47.50
50+2.5mg 10 57.50


1. Alsartan-AM Aristo
Tab. 50+5mg 10 40.00
2. Amlokind-L50+5mg 10 12.50

3.Amlozaar Micro lab

50+5mg 10 55.00
25+5mg 10 32.00
4. Losar-A Unisearch
50+5mg 10 55.00
5. Tozam Torrent
50+5mg 10 55.13

Category : Loop Diuretic , anti-hypertensive
Action : It is a strong diuretic but lacks specific anti-hypertensive action (has no direct
effect on resistance vessels). Thus antihypertensive efficacy is directly related to
diuretic potency. Fall in BP is due only to reduced plasma extracellular fluid
Frusemide inhibits reabsorption of sodium and chloride mainly in the medullary
portion of the ascending limb of the Loop of Henle. Excretion of K+ and
ammonia is also increased while uric acid excretion is reduced. It increases
plasma rennin leveis and secondary hyperaldosteronism may result. Frusemide
reduces BP in hypertensive as well as in normotensives. It reduces pulmonary
oedema before diuresis has set in .

Dosage : Adult : 20-80 mg as single dose. If satisfactory results are not obtained
then 20-40mg after 6 hrs. Infants & children upto 12 yrs : 2 mg/kg bodywt
increased by 1-2 mg/kg 6-8 hrs after the previous dose. Max, 40 mg/day.

LASIX (Frusemide) Sanofi Avents

Tab. 40mg 10 4.72
Inj. 10mg/2ml 1x2ml 2.87
Other combination are:
1. Diucontin-K Modi Mundi
(frusemide + potassium chloride)
Tab. 20+300mg 10 25.45
40+600mg 10 49.25
2. Lasride Sanofi Avents
(Fursemide + Amiloride Hcl)
Tab. 40+5mg 10 11.00

Spironolactone : It is a potassium sparing diuretic having antihypertensive action similar

to thiazides.

Dosage : Adults : 25-200mg daily in single or divided doses.

1. Aldactone RPG
Tab. 25mg 10 18.85
100mg 10 73.76
Other combination are :
1. Fruselac 50+20mg 10 38.81
2. Lasilactone Sanofi Avents
Tab. 50+20mg 10 35.25
2. Spiromide RPG
Tab. 50+20mg 10 23.17

TRIAMTERENE AND AMILORIDE : They are two nonsteroidal organic ases which act
on distal tubule by blocking sodium, potassium and hydrogen exchange. They
decrease potassium excretion. Their action is not dependent on secretion of
aldosterone. Both are used in conjuction with thizide type or high ceiling diuretics
to prevent hypokalemia and slightly augmenthe natriuretic response.
1. Biduret(Amiloride Hcl+Hydrochlorothiazide) Gsk
Tab. 50+50mg 10 22.01
2.Biduret-L GSK
Tab 2.5+25mg 10 12.52
3. Ditide(Triamterene + Benzthiazide) GSK
Tab. 50+25mg 10 29.12
4. Frusemene(Frrusemide + Triamterene) GSK
Tab. 20+50mg 10 19.99
40+50mg 10 24.70

Category : Carbonic Anhydrase Inhibitor; Diuretic
Action : Acetazolamide specially inhibits the enzyme carbonic anhydrase which
catalyses the reversible reaction involving the hydration of carbon dioxide and the
dehydration of carbon acid. In the eye this results in reduced secretion of aqueous
humor and a reduction in intraoculor pressure. In the kidney there is loss of HCO3
ion and, along with it, that of Na+, K+ and water .In CNS acetozolamide exerts an
antiseizure action . It has also been found effective in acute mountain sickness.
Dosage : Epilepsy : 8-30 mg/kg body not daily in div. Doses . Glauma : 250-1 gm daily.
1. Actamide Microvision
Tab. 250mg 10 16.80
2. Diamox Wyeth
Tab. 250mg 10 32.35
3. Avva Intas
Tab. 250mg 10 21.00
Avva SR
Cap. 250mg 10 30.00

Category : Anti-Anginal
Action : Glycery trinitrate relaxes smooth muscle especially in the blood vesseis.
Reduces venous return (preload) and facilities subendocardial blood flow with
redistribution into ischaemic areas. Relieve coronary vasospasm. Dilates arterioles
and reduces afterload. Useful for relief and prevention of anginal attacks. It is a
volatile liquid which is absorbed on the inert matrix of tablet and rendered non

Dosage : Acute attack, 0.5mg every 3 minutes till cessation of pain or limiting side effects
appear. Prophylaxis : 0.5mg prior to activity. To be chewed & not swallowed.
1. Myovin (Nitroglycerine) Cadila
Oint. 2% 30gm 34.00
2. Nitrocontin Modi Mundi
Tab. 2.6mg 25 74.10
6.4mg 25 100.80
3. Nitroject (Nitroglycerine) Sun Pharma
Inj. 5mg/ml 5ml 49.50
10ml 73.50

Category : Potassium Channel Activator; Antianginal
Action : Its antianginal efficacy is mediated through a unique dual mode of action. It
relaxes the vascular smooth muscle, firstly-through membrane hyperpolarisation
via increased transmembrane potassium conductance, and secondly-through an
increase in intracellular cyclic GMP (like nitrates). Its beneficial antianginal effect
is consequent to a combination of increased coronary blood flow via vasodilation
and reduced myocardial oxygen demand via decreased cardiac preload and
afterload. Tolerance is not reported with long-term use of nicorandil. Furthermore
, it exhibites cardioprotective effects via enhancing ischemic preconditioning and
inhibiting free radical activity.

Dosage: Adults : 10-20mg twice daily.

Children : Not recommended.
1. Zynicor Zydus Cadila
Tab. 5mg 20 138.00
10mg 20 198.00
2. Nikoran Torrent
Tab. 5mg 20 139.37
10mg 20 199.96
Nikoran I.V
Inj. 2mg vial 39.99
48mg vial 120.18
3. Korandil Sun
Tab. 5mg 20 139.00
10mg 20 199.60

Category : Nitro Vasodilator; Antianginal
Action : Like all organic nitrates, isosorbide dinitrate relaxes plain muscle. It has no
action on any other tissue. At lower doses this drug dilates venous capacitance
vesseis thereby reducing venous return (preload), conducting arteries and
coronary collaterals. At higher doses arterioles are dilated reducing afterload. In
anginal patients, exercise tolerance and time to one minute. ST depression are
increased. Anginal attacks and intensity are reduced.

Dosages: For quick relief : 5-10mg sublingually.

1. Isordil (Isosrbide dinitrate) Wyeth
Tab. 5mg 100 38.49
10mg 100 43.91
2. Sorbitrate (Isosorbide dinitrate spray) Nicholas
Tab. 5gm 50 28.50
10mg 50 38.93

Category : Nitro Vasidialator + Platelet Inhibitor, Antianginal.
Action : It is more active & longer acting than isosorbide dinitrate. It is effective in
classical as well as variant angia & increase exercise tolerance , postpones ECG
changes of ischaemia.
Isosorbide-5-monontirate (ISMN)and asprin interfere with different regulatory
pathway and thus the combination effective gives a more efficacious and safer
therapeutic option . Combination reduces the chances of GI side effects. Aspirn an
antithrombolic agent is widely used in the prophylaxis of angina and myocardial
infraction. Aspirn induces a long lasting functional detect in platelets, clinically
detectable as prolongation in bleeding time.

Dosages: 20mg 2-3 times a day.

1. Ismo Nocholas
Tab. 10mg 10 19.25
20mg 10 32.00
40mg 7 36.00
2. Imdur Astra Zeneca
Tab. 30mg 10 31.03
60mg 10 49.22
3. Monotrate Sun
Tab. 10mg 10 11.62
20mg 10 21.02
40mg 10 35.59
Tab. S.R. 25mg 10 23.75
S.R. 50mg 10 41.50

Other Combination are :

1.Vaoprin(Isosorbide Mononitrate + Aspirin) Torrent
Tab. 60+150mg 10 42.60
2.Ismorin Nicholas Piramal
Tab. 30+75mg 10 23.50

Category : Antihypertensive Calcium Channel Blocker.
Action : Amlodipine inhibits the movement of calcium ions (Ca2) across the cell
membrane into vascular smooth muscles and mycocytes. Action is greater in the
arterial resistant vessels causing peripheral vasodilation and reduction in
afterload. Action on the myocardium in considerably less. Clinically, blood
pressure is reduced without significant increase in heart rate. In anginal patients
reduction of afteload reduces myocardial oxygen requirement. Sevenrity reduced
while exercise tolerance is increased.

Dosage : 5-10mg once a day.

1. Amlodac(Amlodipine as besylate) Zydus Cadila
Tab. 2.5mg 10 4.95
5mg 10 10.40
10mg 10 15.30
2. Amlokind Mankind
Tab. 2.5mg 10 4.00
5mg 10 5.90
3. Amlopres Cipla
Tab. 2.5mg 10 11.20
5mg 10 20.50
10mg 10 37.45
4. Amlosafe Genetica(Aristo)
Tab. 2.5mg 10 12.83
5mg 10 21.54
10mg 10 36.93
5. Amcard Systopic
Tab. 2.5mg 10 8.50
5mg 10 15.50
10mg 10 27.00
6. Amlogard Pfizer
Tab. 5mg 10 65.00
10mg 10 99.35
7. Calcheka Ipca
Tab. 2.5mg 10 12.00
5mg 10 22.50
10mg 10 43.50
8. Stamlo Dr. Reddy’s
Tab. 2.5mg 10 16.20
5mg 10 24.75
10mg 10 46.35
9. Topdip RPG
Tab. 2.5mg 10 7.90
5mg 10 11.50
10mg 10 20.00
10. Amlocor Torrent
Tab. 2.5mg 10 12.10
5mg 10 20.05
10mg 10 40.20


1. Amlodac –AT (Amlodipine besylate + Atenolol) Zydus Cadila
Tab. 5+50mg 10 27.40
2. Amlokind –AT Mankind
Tab. 5+50mg 10 9.90
3. Amcard –AT Systopic
Tab. 5+50mg 10 24.90
4. Amlopres-AT Cipla
Tab. 5+25mg 10 21.75
5+50mg 10 31.75
5. Tenocheck Ipca
Tab. 5+50mg 10 31.00


1. Amace (Amlodipine besylate + Enalapril Maleate) Systopic
Tab. 5+5mg 10 39.50

Category : Cytoprotective Anti-ischaemic.
Action : Trimetazidine is a cellular acting anti-ischemic agent. It has 3 main properties
by which it acts as a cytoprotective agent. It inhibits the anaerobic glycolysis and fatty
acid metabolism, thus allowing only aerobic glycolysis. This action helps to restore the
energy balance in the cell. It inhibits acidosis and free radical accumulation in the cell.
All these action help the cell to restore the normal ionic and metabolic balance.
Dosages : Adults : 20mg thrice daily after meals. Children : Not recommended.
1. Trivedon (Trimetazidins) Cipla
Tab. 20mg 10 39.25
Trivedon-MR (Trimetazidine dihydrochloride)
35mg 10 60.25
2. Trizidine (Trimetazidine) Nicholas
Tab. 20mg 10 35.00
3. Carvidon Carsyon(Micro lab)
Tab. 20mg 10 36.00

Ginkgo Biloba
Category : Crebral activators
1. Bilovas(Deried extract of Ginkgobiloba) German Remedies
Tab. 40mg 10 70.50
2. Ginvas C.F.L.
Tab. 40mg 10 52.20

Category : Calcium channel blocker; Antiemetic.

Action : Cinnarizine has calcium channel blocking activity selective for arterial smooth
muscle. It has some antithistamine activity. Cinnarizine acts as a labyrinthine sedative. It
also improves microcirculation by reducing ischaemia-induced blood viscocity.

Dosages: Adults : 25-75 mg thrice daily. Children : Not recommended.

1. Cinzan (Cinnarizine) FDC

Tab. 25mg 10 15.00
75mg 10 29.00
2. Cintigo Wallace
Tab. 25mg 10 14.00
Forte 75mg 10 27.00
3. Stugeron Johnson & Johnson
Tab. 25mg 25 58.60
Forte 75mg 20 123.60


Stugil(Cinnarizine + Domperidone) Johnson & Johnson
Tab. 20+15mg 6 33.75

Category : Haemorrheologic Agent
Action : Pentoxyfilline reduces blood viscosity and improves microcirculation and tissue
oxygenation. Erythrocytes become more flexible and can squeeze through narrower

Dosage: 400mg 2-3 times daily. Inj. 15ml by slow i.v infusion in 250-300ml normal
saline over 3 hrs. Repeat 2-3 times daily.
1. Trental Sanofi Aventis
Tab. 400mg 10 26.16
Inj. 300mg 5x15mm 35.47

Category : Haemohtatice / Antiheamorrhagic
Action : Stops haemorrhage from small blood vessels by stabilizing the capillary valls.
Prevention & treatment of capillary haemorrhages associated with (i) Haematemesis,
melena, haemoptysis, haematuria, epistaxis. (ii) menorrhagia, metrorrhagia, post-abortion
& post-partum haeorrhages.

Dosage : Adults : 250-500mg thrice daily. Neonates : 12.5 mg/kg every 6 hrs.
1. Cosklot C.F.L
Tab. 250mg 10 50.00
500mg 10 95.00
Inj. 250mg/2ml 2ml 19.00
2. Alsta Albert David
Tab. 250mg 10 50.71
500mg 10 97.50
Inj. 250mg/2ml 2ml 20.26

ADRENOCHROME MONOSEMICARBA- ZONE : It is believed to reduce capillary

fragility, control oozing from raw surfaces & micro vessel bleeding .

1. Styptovit Dr. Reddy’s

Tab. 10 17.91

2.Sigmachrome Sigma
(Carbazochrome salicylate equation to 5 mg of adrenochrome monosemicarbazone)
Inj. 10ml vial 20.00

FLAVONOIDS : Haemorrhoids, functional venous disorders, varicose veins, IUD

intolerance, menorhagia, metrothagia.
Dosage: 2 tab. Daily, in acute harmorrhoidal attack 6 tab daily.

1.Daflon Serdia
Tab. 500mg 10 147.56

Heparin :
Category : Anticoagulant
Action : Main action is to increase the inhibitory action of antithrombin III (AT III) on
factors XIIa, XIa, Ixa, Xa and thrombin, the major result being inhibition of the
conversion of prothrombin to thrombin. Heparin also inhibits thrombin thus
preventing the conversion of fribringen to fibrin. It has been suggested that at very
low doses heparin reduces postoperative increase in platelet adhesiveness.
Dosage : 5,000-10,000 U every 4-6 hrs. or deep S.C. injection of 25,000 U. every 12-24
hrs. children : 50-100U/kg every 4-6hrs.

1. Heparin Gland Pharama

Inj. Lock Flus 2ml 5.95
5000 I.U/ml 2ml 28.00
25000 I.U/ml 5ml 69.00

2. Beparine Biological. E
Inj. 1000 I.U/ml 5ml 32.52
Inj. 5000 I.U./ml 5ml 98.08

Fraxiparine (Nadroparin) Sanofi Torrent
Inj. 3075 iu 3ml 268.40
4100 iu 4ml 347.80
6ml 389.40
8ml --------

Category : Thrombolytic/ plasminogen activator
Action : Forms a complex with plasminogen which then converts plasminogen to
plasmin. Plasmin breaks down clots as well as fibrionogen and other plasma
proteins. It is obtained from β haemolytic streptococci group c . It is inactive as
such forms a complex with sirculating plasminogen which then causes limited
proteolysis of plasminogen to plasmin. Plasma acts directly on fibrin breaking it
down to achieve thrombolysis.

Dosage : Acute myocardial infraction : I.V 750,000-1.5 million i.u. in 1 hr. Intracoronary:
20,000 i.u. stat followed by 2000-400 i.u./min for 30-90 min. Deep venous &
arterial thrombosis 1.5 million i.u. in 6 hrs.
1. Zykinase Cadila-H.
Inj. 7.5m.i.u vial 2178.32
1.5 m.i.u vial 3898.08
2. Streppaste Sanofi Avents
Inj. 7.5 i.u vial 1395.00
1.5 i.u vial 2497.00
3. Fibrokinase Otsira (Genetica)
Inj. 1.5 i.u vial 2487.00

Category : Thrombolytic Agent
Action : A thrombolytic agent obtained from human kidney cells by tissue culture.
Urokinase directly converse plasminogen into plasmin which then degrades fibrin
clots as well as fibrinogen and other plasma proteins.
1. Urokinase Win-Medicare
Inj. 50,000 i.u. vial 650.00
2,50,000 i.u. vial 1855.80
5,00,000 i.u. vial 3609.90
2. Uni-kinase Unichem
Inj. 250,000 i.u. vial 2080.00
500,000 i.u./ml vial 3690.00
750,000 i.u./ml vial 4800.00
10,00,000 i.u./ml vial 6520.00
3. Solokinase Otsira (Genetic)
Inj. 5.00L vial 3635.00


1. Reopro Elly lilly

Inj. 2mg 5ml vial 19740.00

Category :Platelet inhibitor. Nonsteroidal Anti-inflammatory Drug
Action : Aspirin is an analgesic, anti-inflammatory and antipyretic. This action depends
on the inhibition of the enzyme cyclo-oxygenase in the pathway of prostaglandin
synthesis. Reduction of PG reduces inflammation, pain and fever. Fever is also
reduced by an effect on the hypothalamus. Aspirin inhibits the formation of
thromboxane A2 in the platelets. This inhibits platelet aggregation and
coagulation. This action lasts until the enzyme cyclo-oxygenase is regenerated in
the platelets.
Dosages : 50-100mg daily or as required.
1. Asa 50 (Acetyl salicylic acid) German Remedies
Tab. 50mg 2x14 21.94
2. Delisprin Aristo
Tab. 75mg 10 3.92
150mg 10 6.16
3. Loprin Unisearch
Tab. 75mg 14 3.75
Loprin –DS 162.5mg 14 13.00

Category : Platelet Aggregation inhibitor; Anticoagulant
Action : Clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to
its platelet receptor and the subsequent ADP-mediated activation of the
glycoprotein GP Iib/lla complex, thereby inhibiting platelet aggregation.
Dosage : Adults 75mg once daily with or without blood.
1. Clopigrel USV
Tab. 75mg 10 157.14
2. Deplatt Torrent
Tab. 75mg 10 78.18
3. Clopivas Cipla
Tab. 75mg 10 68.25
Combination with Aspirin
1. Clopigrel –A USV
Tab. 75+75mg 10 157.10
2. Deplatt A (Clopidogrel, Gataprin) Torrent
Tab. 75+75mg 10 78.18
3. Stromix A(Clopidogrel, Aspirin) Nicholas
Tab. 75+75mg 10 87.45

It is a potent inhibitor of platelet aggregation induced by adenosine disphate and it
also inhibits aggregation due to collagen, adrenaline, arachidonic acid, thrombin and
platelet activating factor. When taken orally. Ticlopidine causes a time and dose
dependent inhibitation of both platelet aggregation and release of platelet granule
constitutents, as well as prolongation of bleeding time.
1. Tikleen Ipca
Tab. 250mg 10 85.00
2. Tyklid Torrent
Tab. 250mg 10 95.00
3. Ticlovas USV
Tab. 250mg 10 95.00

Dopamine HCL : It is naturally occurring organic amine. It is much less potent than Adr.
On alpha & beta adregergic (D2) receptors in renal & mesenteric blood vessels, dilates
them .
Dosages : Adults : 2-50 mcg/kg/min can be increased upto 100 mcg/kg/min by slow i.v.
1. Dopacard Nicholas Priamal
Inj. 200 mg/5ml 5ml 26.00
2. Dopamine TTK
Inj. 200 mg/5ml 5ml 22.00

It has a sympathomimetic action. Action of Mephentermine results from an
increasein the cardiac output as well as from peripheral vaso contriction although the
contribution of the latter is negligible.
1. Mephentine Wyeth
Inj. 15mg/ml 1ml 15.91
30mg/ml 10ml 131.33


Though knowledge about the treatment and prevention of heart disease has expanded
dramatically, heart disease remains an immense threat. A total of 925,000 Americans die
each year of cardiovascular disease, a general category which includes heart disease,
stroke, and high blood pressure, all of which are linked. The biggest killer is coronary
heart disease, which claimed 480,170 U.S. deaths in 1992. Stroke and hypertension
together killed about 180,000 and artery diseases killed 40,730.

Many more people suffer than die from heart disease. For example, a total of 5.6 million
Americans had angina pectoris in 1992, and 1,290 people died from it, according to the
AHA. As many as 11.2 million Americans have a history of heart attack, chest pain, or
both. While 39,206 Americans died of heart failure in 1991, more than 800,000
Americans were discharged from the hospital after treatment for the problem in 1992.

Approximately 250,000 Americans die sudden and unexpected deaths due to heart
disease each year, the AHA reports. Such findings support the need for educational efforts
about heart disease and for the expansion of emergency care for heart attack victims.

Genetic therapy for heart disease is considered a fertile area for progress. In 1994,
surgeons performed a procedure on a woman who had a genetic defect that prevented her
liver from removing adequate amounts of LDL cholesterol. She had suffered a heart
attack at age 16. The procedure, which took place in Michigan, involved the insertion of
genetically modified cells in her liver, to enable the organ to remove LDLcholesterol
properly. With the new cells, her heart should no longer be threatened by high levels of

Though much is known about risk factors for heart disease, new theories will continue to
be tested in the future. For example, various studies have shown that individuals who eat
large amounts of fish (especially containing particular oils called omega-3 fatty acids) or
who consume vitamin E have a lower than average rate of coronary heart disease. But
more ambitious studies are needed to confirm this information.

Researchers are also looking carefully at women and heart disease, a topic which has
been overshadowed by research concerning men and heart disease in the past. Estrogen
supplements are known to reduce the risk of heart disease in women, but extensive
studies have not been conducted. The NIH (National Institutes of Health) is currently
funding a long-term study of 27,000 women who will either take estrogen, progesterone,
or a placebo. These women will then be evaluated for heart disease and other indicators.
Such studies will help document what may and may not be helpful to women seeking
protection from heart disease.

In 1998, the American Heart Association published its third list of what it considers to be
the most promising research areas in heart disease. These included: gene therapy which
could potentially encourage the growth of new blood vessels to and from the heart, thus
bypassing diseases vessels; the discovery of new "super aspirins" which seem to have
even greater protective effects for both heart attack and stroke; more data to support the
association between inflammation and heart attacks; better technigues for early detection
of obstructed vessels in the heart (using magnetic resonance imaging, or MRI); hope that
damaged left ventricular muscle can regain better functioning, if a mechanical device
called a left ventricular assist device (LVAD) takes over the work of the left ventricle for
a time; further evidence that tobacco is a crucial risk factor in the development of heart
disease, as evidenced by research which showed that as few as 10 cigarettes a day
shortens life; more research supporting the importance of diet and exercise on levels of
cholesterol in the blood; efforts to encourage people to seek treatment more quickly when
a heart attack is suspected; the association between non-responsiveness to nitric oxide,
and the development of high blood pressure.

Over the past century, researchers have made huge advances in the understanding,
treatment, and prevention of heart disease. For the first time in history, medicine has
acquired the tools to provide many individuals who suffer from heart disease with active,
full lives. Being born with a faulty heart is no longer a reason to live a sedentary,
shortened life. Yet even as the medical profession has gained skill in healing, preserving,
and even replacing the failing heart, this crucial organ remains vulnerable.

New Discoveries would be needed to even consider cardiac surgery.

Anesthesia needed to be improved, the ability to type and cross match blood, with the
invention of blood transfusion. The human ear was no match for the future pictures of
the heart by X-ray and later angiography, the mapping of the coronary arteries. Last the
awesome heart lung machine that would allow prolonged heart surgery.

Until those discoveries were placed together no one was going to attempt to suture the
living heart.

There was a marching progression of discoveries over a hundred-year span that led to the
reinvention of the cardiac surgeon, developed specialty units in hospitals and dispelled
the notion that patients couldn’t survive heart attack. The decline of mortality from heart
attack was literally driven by obsessed individuals. As a group of medical researchers
and inventors they qualify for more outstanding awards that any other related professions
and endeavors, and that includes the Nobel Prize. The modern inventions and discovery
of heart related procedures were going to rock the world’s definition of disease, treatment
and even notions about aging.
The next section summarizes the work of the famed, and the dedicated professionals that
made by-pass a hallmark treatment. The patient was often, the least considered in the
steps to achieve the cooperative goals. It was a scientific and world phenomena still
being studied.


• Schreiber, A., Otto, B., Ju, X., Zenke, M., Goebel, U., Luft, F. C., Kettritz, R.
(2005). Membrane Proteinase 3 Expression in Patients with Wegener's
Granulomatosis and in Human Hematopoietic Stem Cell-Derived Neutrophils. J
Am Soc Nephrol 16: 2216-2224 [Abstract] [Full Text]
• Xiao, H., Heeringa, P., Liu, Z., Huugen, D., Hu, P., Maeda, N., Falk, R. J.,
Jennette, J. C. (2005). The Role of Neutrophils in the Induction of
Glomerulonephritis by Anti-Myeloperoxidase Antibodies. Am J Pathol 167: 39-45
[Abstract] [Full Text]
• Huugen, D., Xiao, H., van Esch, A., Falk, R. J., Peutz-Kootstra, C. J., Buurman,
W. A., Tervaert, J. W. C., Jennette, J. C., Heeringa, P. (2005). Aggravation of Anti-
Myeloperoxidase Antibody-Induced Glomerulonephritis by Bacterial
Lipopolysaccharide: Role of Tumor Necrosis Factor-{alpha}. Am J Pathol 167:
47-58 [Abstract] [Full Text]
• Eisenberger, U., Fakhouri, F., Vanhille, P., Beaufils, H., Mahr, A., Guillevin, L.,
Lesavre, P., Noel, L.-H. (2005). ANCA-negative pauci-immune renal vasculitis:
histology and outcome. Nephrol Dial Transplant 20: 1392-1399 [Abstract] [Full
• Kathiresan, S., Kelsey, P. B., Steere, A. C., Foster, C. S., Curvelo, M. S., Stone, J.
R. (2005). Case 14-2005 - A 38-Year-Old Man with Fever and Blurred Vision.
NEJM 352: 2003-2012 [Full Text]
• Furukawa, Y., Matsumoto, Y., Yamada, M. (2004). Hypertrophic pachymeningitis
as an initial and cardinal manifestation of microscopic polyangiitis. Neurology 63:
1722-1724 [Abstract] [Full Text]
• Tsai, C-N, Chang, C-M, Chuang, C-H, Jin, Y-T, Liu, M-F, Wang, C-R (2004).
Extended colonic ulcerations in a patient with microscopic polyangiitis. Ann
Rheum Dis 63: 1521-1522 [Full Text]
• Yang, J. J., Pendergraft, W. F., Alcorta, D. A., Nachman, P. H., Hogan, S. L.,
Thomas, R. P., Sullivan, P., Jennette, J. C., Falk, R. J., Preston, G. A. (2004).
Circumvention of Normal Constraints on Granule Protein Gene Expression in
Peripheral Blood Neutrophils and Monocytes of Patients with Antineutrophil
Cytoplasmic Autoantibody-Associated Glomerulonephritis. J Am Soc Nephrol 15:
2103-2114 [Abstract] [Full Text]
• Sanders, J.-S. F., van Goor, H., Hanemaaijer, R., Kallenberg, C. G. M., Stegeman,
C. A. (2004). Renal expression of matrix metalloproteinases in human ANCA-
associated glomerulonephritis. Nephrol Dial Transplant 19: 1412-1419 [Abstract]
[Full Text]
• Lock, R J (2004). Rational requesting or rationing testing?. J Clin Pathol 57: 121-
122 [Full Text]
• Borras-Blasco, J., Girona, E., Navarro-Ruiz, A., Matarredona, J., Gimenez, M. E.,
Gutierrez, A., Enriquez, R., Martinez, A. (2004). Acenocoumarol-Induced
Henoch-Schonlein Purpura. Ann Pharmacother 38: 261-264 [Abstract] [Full Text]

• Duran, E., Merkel, P. A., Sweet, S., Swan, N., Babikian, V. L. (2004). ANCA-
associated small vessel vasculitis presenting with ischemic optic neuropathy.
Neurology 62: 152-153 [Full Text]
• Cobeta-Garcia, J. C, Garcia-Enguita, P., Pina-Latorre, M. A, Lerin-Sanchez, F. J,
Rodilla-Calvelo, F. (2004). Ritodrine-Induced Leukocytoclastic Vasculitis in
Pregnancy. Ann Pharmacother 38: 66-69 [Abstract] [Full Text]
• Kroot, E J A, Mak, C L P, Boelhouwer, R U, Middelkoop, M P C, Dees, A (2003).
Involvement of the omentum in Wegener's granulomatosis. Ann Rheum Dis 62:
1238-1239 [Full Text]
• Senf, R., Jurgensen, J. S., Teichgraber, U., Kampf, D., Schindler, R. (2003).
Ruptured arterial aneurysm of the kidney in a patient with Wegener's
granulomatosis. Nephrol Dial Transplant 18: 2671-2673 [Full Text]
• Rarok, A. A., Limburg, P. C., Kallenberg, C. G. M. (2003). Neutrophil-activating
potential of antineutrophil cytoplasm autoantibodies. J Leukoc Biol 74: 3-15
[Abstract] [Full Text]
• Slart, R H J A, Jager, P L, Poot, L, Piers, D A, Cohen Tervaert, J-W, Stegeman, C
A (2003). Clinical value of gallium-67 scintigraphy in assessment of disease
activity in Wegener's granulomatosis. Ann Rheum Dis 62: 659-662 [Abstract]
[Full Text]
• Papi, M., De Pita, O., Frezzolini, A., Didona, B., Sais, G., Vidaller, A. (1999).
Prognostic Factors in Leukocytoclastic Vasculitis: What Is the Role of
Antineutrophil Cytoplasmic Antibody?. Arch Dermatol 135: 714-715 [Full Text]
• Anthony, D. D., Askari, A. D., Wolpaw, T., McComsey, G. (1999). Wegener
Granulomatosis Simulating Bacterial Endocarditis. Arch Intern Med 159: 1807-
1810 [Abstract] [Full Text]
• Coblyn, J. S., McCluskey, R. T. (2003). Case 3-2003 - A 36-Year-Old Man with
Renal Failure, Hypertension, and Neurologic Abnormalities. NEJM 348: 333-342
[Full Text]
• Bhullar, N., Folzenlogen, D. D. (2002). Henoch-Schonlein Purpura: Upper
Respiratory Tract Infection or Drug Induced?. Arch Intern Med 162: 222-223
[Full Text]
• Scholzen, T. E., Sunderkotter, C., Kalden, D.-H., Brzoska, T., Fastrich, M.,
Fisbeck, T., Armstrong, C. A., Ansel, J. C., Luger, T. A. (2003). {alpha}-
Melanocyte Stimulating Hormone Prevents Lipopolysaccharide-Induced
Vasculitis by Down-Regulating Endothelial Cell Adhesion Molecule Expression.
Endocrinology 144: 360-370 [Abstract] [Full Text]

• Utzig, M. J., Warzelhan, J., Wertzel, H., Berwanger, I., Hasse, J. (2002). Role of
thoracic surgery and interventional bronchoscopy in Wegener's granulomatosis.
Ann. Thorac. Surg. 74: 1948-1952 [Abstract] [Full Text]
• Xiao, H., Heeringa, P., Hu, P., Liu, Z., Zhao, M., Aratani, Y., Maeda, N., Falk, R.
J., Jennette, J. C. (2002). Antineutrophil cytoplasmic autoantibodies specific for
myeloperoxidase cause glomerulonephritis and vasculitis in mice. J. Clin. Invest.
110: 955-963 [Abstract] [Full Text]
• O'Sullivan, B. P., Erickson, L. A., Niles, J. L. (2002). Case 30-2002 - An Eight-
Year-Old Girl with Fever, Hemoptysis, and Pulmonary Consolidations. NEJM
347: 1009-1017 [Full Text]
• Helfgott, S. M., Smith, R. N. (2002). Case 21-2002 - A 21-Year-Old Man with
Arthritis during Treatment for Hyperthyroidism. NEJM 347