¹ 5. Work
of the Heart. The Heart Sounds.
Because the heart is composed primarily of cardiac muscle tissue that
continuously contracts and relaxes, it must have a constant supply of oxygen
and nutrients. The coronary arteries are the network of blood vessels that
carry oxygen- and nutrient-rich blood to the cardiac muscle tissue.
The blood
leaving the left ventricle exits through the aorta, the body’s main artery. Two
coronary arteries, referred to as the "left" and "right"
coronary arteries, emerge from the beginning of the aorta, near the top of the
heart.
The initial
segment of the left coronary artery is called the left main coronary. This
blood vessel is approximately the width of a soda straw and is less than an
inch long. It branches into two slightly smaller arteries: the left anterior
descending coronary artery and the left circumflex coronary artery. The left
anterior descending coronary artery is embedded in the surface of the front
side of the heart. The left circumflex coronary artery circles around the left
side of the heart and is embedded in the surface of the back of the heart.
Just like
branches on a tree, the coronary arteries branch into progressively smaller
vessels. The larger vessels travel along the surface of the heart; however, the
smaller branches penetrate the heart muscle. The smallest branches, called
capillaries, are so narrow that the red blood cells must travel in single file.
In the capillaries, the red blood cells provide oxygen and nutrients to the
cardiac muscle tissue and bond with carbon dioxide and other metabolic waste
products, taking them away from the heart for disposal through the lungs,
kidneys and liver.
When
cholesterol plaque accumulates to the point of blocking the flow of blood
through a coronary artery, the cardiac muscle tissue fed by the coronary artery
beyond the point of the blockage is deprived of oxygen and nutrients. This area
of cardiac muscle tissue ceases to function properly. The condition when a
coronary artery becomes blocked causing damage to the cardiac muscle tissue it
serves is called a myocardial infarction or heart attack.
The superior
vena cava is one of the two main veins bringing de-oxygenated blood from the
body to the heart. Veins from the head and upper body feed into the superior
vena cava, which empties into the right atrium of the heart.
The inferior
vena cava is one of the two main veins bringing de-oxygenated blood from the
body to the heart. Veins from the legs and lower torso feed into the inferior
vena cava, which empties into the right atrium of the heart.
Schematic view of the aorta and a number of its most important branches
The aorta is
the largest single blood vessel in the body. It is approximately the diameter
of your thumb. This vessel carries oxygen-rich blood from the left ventricle to
the various parts of the body.
In anatomical sources, the aorta is usually divided into sections. One way
of classifying a part of the aorta is by anatomical compartment, where the thoracic
aorta (or thoracic part of the aorta) runs from the heart to the thoracic
diaphragm. The aorta then continues as the abdominal aorta (or abdominal part
of the aorta) diaphragm to the aortic bifurcation. Another system divides the
aorta with respect to its course and the direction of blood flow. In this
system, the aorta starts as the ascending aorta (or ascending part of the
aorta), taking a superior course from the heart, but then making a hairpin
turn, the aortic arch or arch of aorta. The part after this hairpin turn takes
an inferior course and is known as the descending aorta (or descending part of
the aorta). The aorta ends by dividing into two major blood vessels, the common
iliac arteries and a smaller midline vessel, the median sacral artery.:18
The aorta supplies all of the systemic circulation, which means that the
entire body, except for the respiratory zone of the lung gets its blood from
the aorta. Broadly speaking, branches from the ascending aorta supply the
heart, branches from the aortic arch supply the head, neck and arms, branches
from the thoracic descending aorta supply the chest (excluding the heart and
the respiratory zone of the lung) and branches from the abdominal aorta supply
the abdomen. The pelvis and legs get their blood from the common iliac
arteries.
Ascending aorta
The ascending aorta originates at the orifice of the aortic valve. It runs
in a common pericardial sheath with the pulmonary trunk. These two blood
vessels twist around each other, so that the aorta starts out posterior to the
pulmonary trunk, but then twists to its right and anterior side. :191, 204 The transition from ascending aorta to aortic arch
is at the pericardial reflection on the aorta. :Plate
211
At the root of the ascending aorta, the lumen has three little pockets
between the cusps of the aortic valve and the wall of the aorta, named the
aortic sinuses or sinuses of Valsalva. The left aortic sinus contains the
origin of the left coronary artery and the right aortic sinus likewise gives
rise to the right coronary artery. Together, these two arteries normally supply
the heart. The posterior aortic sinus does not give rise to a coronary artery.
For this reason, the left, right and posterior aortic sinuses are also called
left-coronary, right-coronary and non-coronary sinuses:191
Aortic arch
The aortic arch loops over the right pulmonary artery and the bifurcation
of the pulmonary trunk, with which it remains connected by the ligamentum
arteriosum, a remnant of the fetal circulation that is obliterated a few days
after birth. In addition to these blood vessels, the aortic arch crosses the
left main bronchus. Between it and the pulmonary trunk is a network of
autonomic nerve fibers, the cardiac or aortic plexus. The left vagus nerve,
which passes anterior to the aortic arch, gives off a major branch, the
recurrent laryngeal nerve, which loops under the aortic arch just lateral to
the ligamentum arteriosum. It then runs back to the neck.
The aortic arch has three major branches: from proximal to distal they are
the brachiocephalic trunk, which supplies the right side of the head and neck,
as well as the right arm and chest wall, the left common carotid artery, the
left common carotid artery and the left subclavian artery. The latter two
together supply the left side of the same regions.
At the level of the intervertebral disc between the fourth and fifth
thoracic vertebrae, the aortic arch ends and the descending aorta starts.:209
Thoracic descending aorta
The thoracic descending aorta gives rise to the intercostal and subcostal
arteries, as well as to the superior and inferior left bronchial arteries and
variable branches to the oesophagus, mediastinum, and pericardium. Its lowest
pair of branches is are the superior phrenic arteries,
which supply the diaphragm.
Abdominal descending aorta
The abdominal aorta gives rise to lumbar and musculophrenic arteries, renal
and middle suprarenal arteries, and visceral arteries (the celiac trunk, the
superior mesenteric artery and the inferior mesenteric artery). It ends in a
bifurcation into the left and right common iliac arteries. At the point of the
bifurcation, there also springs a smaller branch, the median sacral artery.
In other animals
All amniotes have a broadly similar arrangement to that of humans, albeit
with a number of individual variations. In fish, however, there are two
separate vessels referred to as aortas. The ventral aorta carries de-oxygenated
blood from the heart to the gills; part of this vessel forms the ascending
aorta in tetrapods (the remainder forms the pulmonary artery). A second, dorsal
aorta carries oxygenated blood from the gills to the rest of the body, and is
homologous with the descending aorta of tetrapods. The two aortas are connected
by a number of vessels, one passing through each of the gills. Amphibians also
retain the fifth connecting vessel, so that the aorta has two parallel arches.
Embryological development
In mammalian and avian embryological development, the pharyngeal arch
(aortic arches) arteries contribute to the normal pattern of the great
arteries. The fourth aortic arch vessel survives in these vertebrates as the
arch of the aorta, the third aortic arch vessel persists as the brachiocephalic
artery or the root of the internal carotid, and the sixth arch contributes to
the pulmonary arteries. The smooth muscle of the great arteries and the
population of cells that form the aorticopulmonary septum that separates the
aorta and pulmonary artery is derived from cardiac
neural crest. This contribution of the neural crest to the great artery smooth
muscle is unusual as most smooth muscle is derived from mesoderm. In fact the
smooth muscle within the abdominal aorta is derived from mesoderm, and the
coronary arteries, which arise just above the semilunar valves, possess smooth
muscle of mesodermal origin. A failure of the aorticopulmonary septum to divide
the great vessels results in persistent truncus arteriosus.
Features
The aorta is an elastic artery, and as such is quite distensible. Mean
arterial blood pressure is highest in the aorta and mean arterial pressure
diminishes across the circulation from aorta to arteries to arterioles to
capillaries to veins back to atrium: the difference between aortic and right
atrial pressure accounts for blood flow in the circulation. The aorta consists
of a heterogeneous mixture of smooth muscle, nerves, intimal cells, endothelial
cells, fibroblast-like cells, and a complex extracellular matrix. The vascular
wall consists of several layers known as the tunica adventitia, tunica media,
and tunica intima. The thickness of the aorta encourages an extensive network
of tiny blood vessels called vasa vasorum, which feed the outer layers of the
aorta. The aortic arch contains baroreceptors and chemoreceptors that relay
information concerning blood pressure and blood pH and carbon dioxide levels to
the medulla oblongata of the brain. This information is processed by the brain
and the autonomic nervous system mediates the homeostatic responses.
Within the tunica media, smooth muscle and the extracellular matrix are
quantitatively the largest components of the aortic vascular wall. The
fundamental unit of the aorta is the elastic lamella, which consists of smooth
muscle and elastic matrix. The medial layer of the aorta
consist of concentric musculoelastic layers (the elastic lamella) in
mammals. The smooth muscle component does not dramatically alter the diameter
of the aorta but rather serves to increase the stiffness and viscoelasticity of
the aortic wall when activated. The elastic matrix dominates the biomechanical
properties of the aorta. The elastic matrix forms lamella, consisting of
elastic fibers, collagens(predominately type III),
proteoglycans, and glycoaminoglycans. When the left ventricle contracts to
force blood into the aorta, the aorta expands. This stretching gives the
potential energy that will help maintain blood pressure during diastole, as
during this time the aorta contracts passively. This Windkessel effect of the
great elastic arteries has important biomechanical implications. The elastic recoil
helps conserve the energy from the pumping heart and smooth out the pulsatile
nature created by the heart. Aortic pressure is highest at the aorta and
becomes less pulsatile and lower pressure as blood vessels divide into
arteries, arterioles, and capillaries such that flow is slow and smooth for
gases and nutrient exchange.
Blood flow and velocity
The pulsatile nature of blood flow creates a pulse wave that is propagated
down the arterial tree, and at bifurcations reflected waves rebound to return to
semilunar valves and the origin of the aorta. These return waves create the
dicrotic notch displayed in the aortic pressure curve during the cardiac cycle
as these reflected waves push on the aortic semilunar valve. With age, the
aorta stiffens such that the pulse wave is propagated faster and reflected
waves return to the heart faster before the semilunar valve closes, which
raises the blood pressure. The stiffness of the aorta is associated with a
number of diseases and pathologies, and noninvasive measures of the pulse wave
velocity are an independent indicator of hypertension. Measuring the pulse wave
velocity (invasively and non-invasively) is a means of determining arterial
stiffness. Maximum aortic velocity may be noted as Vmax or less commonly as AoVmax.
The
pulmonary artery is the vessel transporting de-oxygenated blood from the right
ventricle to the lungs. A common misconception is that all arteries carry
oxygen-rich blood. It is more appropriate to classify arteries as vessels carrying
blood away from the heart.
The
pulmonary vein is the vessel transporting oxygen-rich blood from the lungs to
the left atrium. A common misconception is that all veins carry de-oxygenated
blood. It is more appropriate to classify veins as vessels carrying blood to
the heart.
The right
atrium receives de-oxygenated blood from the body through the superior vena
cava (head and upper body) and inferior vena cava (legs and lower torso). The
sinoatrial node sends an impulse that causes the cardiac muscle tissue of the
atrium to contract in a coordinated, wave-like manner. The tricuspid valve,
which separates the right atrium from the right ventricle, opens to allow the
de-oxygenated blood collected in the right atrium to flow into the right
ventricle.
The right
ventricle receives de-oxygenated blood as the right atrium contracts. The
pulmonary valve leading into the pulmonary artery is closed, allowing the
ventricle to fill with blood. Once the ventricles are full, they contract. As
the right ventricle contracts, the tricuspid valve closes and the pulmonary
valve opens. The closure of the tricuspid valve prevents blood from backing
into the right atrium and the opening of the pulmonary valve allows the blood
to flow into the pulmonary artery toward the lungs.
The left
atrium receives oxygenated blood from the lungs through the pulmonary vein. As
the contraction triggered by the sinoatrial node progresses through the atria,
the blood passes through the mitral valve into the left ventricle.
The left
ventricle receives oxygenated blood as the left atrium contracts. The blood
passes through the mitral valve into the right ventricle. The aortic valve
leading into the aorta is closed, allowing the ventricle to fill with blood.
Once the ventricles are full, they contract. As the left ventricle contracts,
the mitral valve closes and the aortic valve opens. The closure of the mitral
valve prevents blood from backing into the left atrium and the opening of the
aortic valve allows the blood to flow into the aorta and flow throughout the
body.
The
papillary muscles attach to the lower portion of the interior wall of the
ventricles. They connect to the chordae tendineae, which attach to the
tricuspid valve in the right ventricle and the mitral valve in the left
ventricle. The contraction of the papillary muscles opens these valves. When
the papillary muscles relax, the valves close.
The chordae
tendineae are tendons linking the papillary muscles to the tricuspid valve in
the right ventricle and the mitral valve in the left ventricle. As the
papillary muscles contract and relax, the chordae tendineae transmit the
resulting increase and decrease in tension to the respective valves, causing
them to open and close. The chordae tendineae are string-like in appearance and
are sometimes referred to as "heart strings."
The
tricuspid valve separates the right atrium from the right ventricle. It opens
to allow the de-oxygenated blood collected in the right atrium to flow into the
right ventricle. It closes as the right ventricle contracts, preventing blood
from returning to the right atrium; thereby, forcing it to exit through the
pulmonary valve into the pulmonary artery.
The mitral
valve separates the left atrium from the left ventricle. It opens to allow the
oxygenated blood collected in the left atrium to flow into the left ventricle.
It closes as the left ventricle contracts, preventing blood from returning to
the left atrium; thereby, forcing it to exit through the aortic valve into the
aorta.
The
pulmonary valve separates the right ventricle from the pulmonary artery. As the
ventricles contract, it opens to allow the de-oxygenated blood collected in the
right ventricle to flow to the lungs. It closes as the ventricles relax,
preventing blood from returning to the heart.
The aortic
valve separates the left ventricle from the aorta. As the ventricles contract,
it opens to allow the oxygenated blood collected in the left ventricle to flow
throughout the body. It closes as the ventricles relax, preventing blood from
returning to the heart.
ADDITIONAL
INFORMATION
THORACIC CAVITY
The lungs and heart are located in the thoracic cavity.
THE HEART
The heart is the simplest organ in the body. It does only one thing:
pumps blood. It beats 42 million times a year. It’s about the size
of your clenched fist. (Show life-size model of heart). Some of
you have big fists, some have smaller fists. Its location is deep to the
sternum. Take your fist and place it on the sternum, then angle the
bottom of your wrist to the left. When you say the Pledge of Allegiance,
your hand is not over your heart. It’s not on the left, it’s in the
center.
HEART BEATS
The pressure of blood against blood vessel walls is called blood pressure.
Blood pressure is recorded systole over diastole. Normal resting blood
pressure is said to be 120/80.
When blood pressure is too high, it is called HYPERTENSION.
The sound your heart makes when it is beating is the sound of the valves
closing.
The heart normally beats at a rate of 60-80 beats per minute. A faster or slower heart rate is an indication of a problem.
ARRHYTHMIA = improper heart beat; needs
medicines or a pacemaker.
FIBRILLATION is when the heart beat is
rapid and dangerously uncoordinated, and doesn’t contract rhythmically and
just quivers without pumping blood. It needs an electric shock from a
defibrillator. This machine is never used when someone’s heart is beating, even
irregularly, because it can cause the heart to stop. Whatever caused the
fibrillation in the first place is not treated, so it may not work, but it’s
worth a try! Most large public facilities have them. There are three on
this campus. Disneyland has one every 100 yards.
THE HEART NEEDS ITS OWN BLOOD/O2
The blood vessels for the actual muscle that makes up the heart comes from
vessels that are on the outside of the heart = CORONARY ARTERIES.
The more you exercise, the more branches of these arteries are formed, and
the better the blood supply to the heart. Blockage in the coronary arteries is
called a heart attack.
For a narrow artery, you can do a CORONARY BYPASS. Take
another blood vessel graft (from thigh) and go around the blockage. For
double or triple bypasses, that’s how many vessels are affected.
HEART ATTACK
Severe pain from lack of blood to the heart is called ANGINA.
If there is complete blockage à not enough O2 to that area à that part of heart muscle dies = MYOCARDIAL INFARCTION= HEART ATTACK.
Heart muscle never regenerates. If a large area dies, person will die.
What are symptoms of a heart attack? Besides chest pain or pressure,
symptoms can include pain down left arm, shortness of breath, nausea, feeling of indigestion or heartburn, even pain in the
jaw that is mistaken for a toothache. A common symptom is death.
50% of first heart attacks are fatal. About ¾ million people die each
year from heart attacks.
Reasons for blockage
ATHEROSCLEROSIS = build-up
of fat inside artery (called a PLAQUE) à narrowing of artery à blood clot. If
clot is big, it can break off and go to the lungs. When a clot lodges in an
artery, all the tissue beyond that point gets deprived of oxygen and dies.
BLOOD VESSELS
There are 100,000 miles of blood vessels.
With the exception of cartilage (which does not have a blood supply, no
cell in the body is more than a few cell diameters away from a blood vessel, so
they can get oxygen, nutrients, remove waste.
Arteries get smaller and
thinner and are then called arterioles.
Arterioles get smaller and thinner until they are just one cell thick. At
this point, they are called capillaries, and this is where the oxygen exchange
takes place. Capillaries then get larger as they take waste products away from
the cells in the capillary bed and head back to the heart; now they are called
venules. As venules get bigger, they are called veins until they return to the
heart. From the heart the blood is pumped to the lungs to get more oxygen.
During this trip, they get smaller again until they are capillaries, then they
get the oxygen from the lungs and drop off the waste products (carbon dioxide).
Then the blood returns to the heart to get pumped out to the body again.
CAPILLARIES are the only
sites of nutrient, gas exchange, and waste exchange in the cardiovascular
system.
Veins are the only blood vessels that have valves. Allows
blood to move in only one direction. What pushes the blood?
The muscle of the body constrict, squeezes the vessels.
LYMPHATIC VESSELS
You have a whole network of arteries. You have a whole network of veins.
You have a whole network of lymph vessels. Lymph vessels look like veins and
also have valves.
The lymph system retrieves excess tissue fluid (plasma that leaks out of
the blood vessels) and filters it and cleans it and returns it to the blood. This plasma is now called lymphatic fluid. It is sent through the lymph
nodes through out the body. There are hundreds of lymph nodes in the body,
occurring in clusters. Each lymph node filters the lymph fluid to get rid
of bacteria and viruses, and returns the fluid back into the blood.
There are large clusters of lymph nodes in the armpit, neck, and
groin regions.
The lymph that filters the breast area will drain into the nodes in the
armpit, so that is where cancer would spread first. It is detected by
lymph node biopsy. If cancer is found, the surgeon will have to remove
all the lymph nodes from the armpit, and afterwards, there is no lymph drainage
for that arm, and there will be problems with swelling.
GIANT LYMPH NODES
The SPLEEN not only destroys old red blood cells, it is also a giant
lymph node.
TONSILS are also lymph nodes, but
they can be removed if they are chronically infected.
The cardiovascular system
The cardiovascular system consists of the heart, blood vessels, and the
approximately 5 liters of blood that the blood vessels transport. Responsible
for transporting oxygen, nutrients, hormones, and cellular waste products
throughout the body, the cardiovascular system is powered by the body’s
hardest-working organ — the heart, which is only about the size of a closed
fist. Even at rest, the average heart easily pumps over 5 liters of blood
throughout the body every minute.
The Heart
The heart is a muscular pumping organ located medial to the lungs along the
body’s midline in the thoracic region. The bottom tip of the heart, known as
its apex, is turned to the left, so that about 2/3 of the heart is located on the
body’s left side with the other 1/3 on right. The top of the heart, known as
the heart’s base, connects to the great blood vessels of the body: the aorta,
vena cava, pulmonary trunk, and pulmonary veins.
Anatomy of the Heart
Pericardium
The heart sits within a fluid-filled cavity called the pericardial cavity.
The walls and lining of the pericardial cavity are a special membrane known as
the pericardium. Pericardium is a type of serous membrane that produces serous
fluid to lubricate the heart and prevent friction between the ever beating
heart and its surrounding organs. Besides lubrication, the pericardium serves
to hold the heart in position and maintain a hollow space for the heart to
expand into when it is full. The pericardium has 2 layers—a visceral layer that
covers the outside of the heart and a parietal layer that forms a sac around
the outside of the pericardial cavity.
Structure of the Heart Wall
The heart wall is made of 3 layers: epicardium, myocardium and endocardium.
Epicardium. The
epicardium is the outermost layer of the heart wall and is just another name
for the visceral layer of the pericardium. Thus, the epicardium is a thin layer
of serous membrane that helps to lubricate and protect the outside of the
heart. Below the epicardium is the second, thicker layer of the heart wall: the
myocardium.
Myocardium. The
myocardium is the muscular middle layer of the heart wall that contains the
cardiac muscle tissue. Myocardium makes up the majority of the thickness and
mass of the heart wall and is the part of the heart responsible for pumping
blood. Below the myocardium is the thin endocardium layer.
Endocardium. Endocardium
is the simple squamous endothelium layer that lines the inside of the heart.
The endocardium is very smooth and is responsible for keeping blood from
sticking to the inside of the heart and forming potentially deadly blood clots.
The thickness of the heart wall varies in different parts of the heart. The
atria of the heart have a very thin myocardium because they do not need to pump
blood very far—only to the nearby ventricles. The ventricles, on the other
hand, have a very thick myocardium to pump blood to the lungs or throughout the
entire body. The right side of the heart has less myocardium in its walls than
the left side because the left side has to pump blood through the entire body
while the right side only has to pump to the lungs.
Chambers of the Heart
The heart contains 4 chambers: the right atrium, left atrium, right
ventricle, and left ventricle. The atria are smaller than the ventricles and
have thinner, less muscular walls than the ventricles. The atria act as
receiving chambers for blood, so they are connected to the veins that carry
blood to the heart. The ventricles are the larger, stronger pumping chambers
that send blood out of the heart. The ventricles are connected to the arteries
that carry blood away from the heart.
The chambers on the right side of the heart are smaller and have less
myocardium in their heart wall when compared to the left side of the heart.
This difference in size between the sides of the heart is related to their
functions and the size of the 2 circulatory loops. The right side of the heart
maintains pulmonary circulation to the nearby lungs while the left side of the
heart pumps blood all the way to the extremities of the body in the systemic
circulatory loop.
Valves of the Heart
The heart functions by pumping blood both to the lungs and to the systems
of the body. To prevent blood from flowing backwards or “regurgitating” back
into the heart, a system of one-way valves are present in the heart. The heart
valves can be broken down into two types: atrioventricular and semilunar
valves.
Atrioventricular valves. The
atrioventricular (AV) valves are located in the middle of the heart between the
atria and ventricles and only allow blood to flow from the atria into the
ventricles. The AV valve on the right side of the heart is called the tricuspid
valve because it is made of three cusps (flaps) that separate to allow blood to
pass through and connect to block regurgitation of blood. The AV valve on the
left side of the heart is called the mitral valve or the bicuspid valve because
it has two cusps. The AV valves are attached on the ventricular side to tough
strings called chordae tendineae. The chordae tendineae pull on the AV valves
to keep them from folding backwards and allowing blood to regurgitate past
them. During the contraction of the ventricles, the AV valves look like domed
parachutes with the chordae tendineae acting as the ropes holding the
parachutes taut.
Semilunar valves. The
semilunar valves, so named for the crescent moon shape of their cusps, are
located between the ventricles and the arteries that carry blood away from the
heart. The semilunar valve on the right side of the heart is the pulmonary
valve, so named because it prevents the backflow of blood from the pulmonary
trunk into the right ventricle. The semilunar valve on the left side of the
heart is the aortic valve, named for the fact that it prevents the aorta from
regurgitating blood back into the left ventricle. The semilunar valves are
smaller than the AV valves and do not have chordae tendineae to hold them in
place. Instead, the cusps of the semilunar valves are cup shaped to catch
regurgitating blood and use the blood’s pressure to snap shut.
Conduction System of the Heart
The heart is able to both set its own rhythm and to conduct the signals
necessary to maintain and coordinate this rhythm throughout its structures.
About 1% of the cardiac muscle cells in the heart are responsible for forming
the conduction system that sets the pace for the rest of the cardiac muscle
cells.
The conduction system starts with the pacemaker of the heart—a small bundle
of cells known as the sinoatrial (SA) node. The SA node is located in the wall
of the right atrium inferior to the superior vena cava. The SA node is
responsible for setting the pace of the heart as a whole and directly signals
the atria to contract. The signal from the SA node is picked up by another mass
of conductive tissue known as the atrioventricular (AV) node.
The AV node is located in the right atrium in the inferior portion of
the interatrial septum. The AV node picks up the signal sent by the SA node and
transmits it through the atrioventricular (AV) bundle. The AV bundle is a
strand of conductive tissue that runs through the interatrial septum and into
the interventricular septum. The AV bundle splits into left and right branches
in the interventricular septum and continues running through the septum until
they reach the apex of the heart. Branching off from the left and right bundle
branches are many Purkinje fibers that carry the signal to the walls of the
ventricles, stimulating the cardiac muscle cells to contract in a coordinated
manner to efficiently pump blood out of the heart.
Physiology of the Heart
Coronary Systole and Diastole
At any given time the chambers of the heart may found in one of two states:
Systole. During systole, cardiac
muscle tissue is contracting to push blood out of the chamber.
Diastole. During diastole, the cardiac
muscle cells relax to allow the chamber to fill with blood. Blood pressure
increases in the major arteries during ventricular systole and decreases during
ventricular diastole. This leads to the 2 numbers associated with blood
pressure—systolic blood pressure is the higher number and diastolic blood
pressure is the lower number. For example, a blood pressure of 120/80 describes
the systolic pressure (120) and the diastolic pressure (80).
The Cardiac Cycle
The cardiac cycle includes all of the events that take place during one
heartbeat. There are 3 phases to the cardiac cycle: atrial systole, ventricular
systole, and relaxation.
Atrial systole: During the atrial systole phase of the cardiac cycle, the
atria contract and push blood into the ventricles. To facilitate this filling,
the AV valves stay open and the semilunar valves stay closed to keep arterial
blood from re-entering the heart. The atria are much smaller than the
ventricles, so they only fill about 25% of the ventricles during this phase.
The ventricles remain in diastole during this phase.
Ventricular systole: During ventricular systole, the ventricles contract to
push blood into the aorta and pulmonary trunk. The pressure of the ventricles
forces the semilunar valves to open and the AV valves to close. This
arrangement of valves allows for blood flow from the ventricles into the
arteries. The cardiac muscles of the atria repolarize and enter the state of
diastole during this phase.
Relaxation phase: During the relaxation phase, all 4 chambers of the
heart are in diastole as blood pours into the heart from the veins. The
ventricles fill to about 75% capacity during this phase and will be completely
filled only after the atria enter systole. The cardiac muscle cells of the
ventricles repolarize during this phase to prepare for the next round of
depolarization and contraction. During this phase, the AV valves open to allow
blood to flow freely into the ventricles while the semilunar valves close to
prevent the regurgitation of blood from the great arteries into the ventricles.
Blood Flow through the Heart
Deoxygenated blood returning from the body first enters the heart from the
superior and inferior vena cava. The blood enters the right atrium and is
pumped through the tricuspid valve into the right ventricle. From the right
ventricle, the blood is pumped through the pulmonary semilunar valve into the
pulmonary trunk.
The pulmonary trunk carries blood to the lungs where it releases
carbon dioxide and absorbs oxygen. The blood in the lungs returns to the heart
through the pulmonary veins. From the pulmonary veins, blood enters the heart
again in the left atrium.
The left atrium contracts to pump blood through the bicuspid (mitral)
valve into the left ventricle. The left ventricle pumps blood through the
aortic semilunar valve into the aorta. From the aorta, blood enters into
systemic circulation throughout the body tissues until it returns to the heart
via the vena cava and the cycle repeats.
The Electrocardiogram
The electrocardiogram (also known as an EKG or ECG) is a non-invasive
device that measures and monitors the electrical activity of the heart through
the skin. The EKG produces a distinctive waveform in response to the electrical
changes taking place within the heart.
The first part of the wave, called the P wave, is a small increase in
voltage of about 0.1 mV that corresponds to the depolarization of the atria
during atrial systole. The next part of the EKG wave is the QRS complex which
features a small drop in voltage (Q) a large voltage peak (R) and another small
drop in voltage (S). The QRS complex corresponds to the depolarization of the
ventricles during ventricular systole. The atria also repolarize during the QRS
complex, but have almost no effect on the EKG because they are so much smaller
than the ventricles.
The final part of the EKG wave is the T wave, a small peak that
follows the QRS complex. The T wave represents the ventricular repolarization
during the relaxation phase of the cardiac cycle. Variations in the waveform
and distance between the waves of the EKG can be used clinically to diagnose
the effects of heart attacks, congenital heart problems, and electrolyte
imbalances.
HEART SOUNDS
The sounds of a normal heartbeat are known as “lubb” and “dupp” and are
caused by blood pushing on the valves of the heart. The “lubb” sound comes
first in the heartbeat and is the longer of the two heart sounds. The “lubb”
sound is produced by the closing of the AV valves at the beginning of
ventricular systole. The shorter, sharper “dupp” sound is similarly caused by
the closing of the semilunar valves at the end of ventricular systole. During a
normal heartbeat, these sounds repeat in a regular pattern of lubb-dupp-pause.
Any additional sounds such as liquid rushing or gurgling indicate a structure
problem in the heart. The most likely causes of these extraneous sounds are
defects in the atrial or ventricular septum or leakage in the valves.
Cardiac Output
Cardiac output (CO) is the volume of blood being pumped by the heart in one
minute. The equation used to find cardiac output is: CO = Stroke Volume x Heart
Rate
Stroke volume is the amount of blood pumped into the aorta during
each ventricular systole, usually measured in milliliters. Heart rate is the
number of heartbeats per minute. The average heart can push around 5 to 5.5
liters per minute at rest.
Circulatory Loops
There are 2 primary circulatory loops in the human body: the pulmonary
circulation loop and the systemic circulation loop.
Pulmonary circulation transports deoxygenated blood from the right side of
the heart to the lungs, where the blood picks up oxygen and returns to the left
side of the heart. The pumping chambers of the heart that support the pulmonary
circulation loop are the right atrium and right ventricle.
Systemic circulation carries highly oxygenated blood from the left
side of the heart to all of the tissues of the body (with the exception of the
heart and lungs). Systemic circulation removes wastes from body tissues and
returns deoxygenated blood to the right side of the heart. The left atrium and
left ventricle of the heart are the pumping chambers for the systemic
circulation loop.
Blood Vessels
Blood vessels are the body’s highways that allow blood to flow quickly and
efficiently from the heart to every region of the body and back again. The size
of blood vessels corresponds with the amount of blood that passes through the
vessel. All blood vessels contain a hollow area called the lumen through which
blood is able to flow. Around the lumen is the wall of the vessel, which may be
thin in the case of capillaries or very thick in the case of arteries.
All blood vessels are lined with a thin layer of simple squamous
epithelium known as the endothelium that keeps blood cells inside of the blood
vessels and prevents clots from forming. The endothelium lines the entire
circulatory system, all the way to the interior of the heart, where it is
called the endocardium.
There are three major types of blood vessels: arteries, capillaries
and veins. Blood vessels are often named after either the region of the body
through which they carry blood or for nearby structures. For example, the
brachiocephalic artery carries blood into the brachial (arm) and cephalic
(head) regions. One of its branches, the subclavian artery, runs under the
clavicle; hence the name subclavian. The subclavian artery runs into the
axillary region where it becomes known as the axillary artery.
Arteries and Arterioles: Arteries are blood vessels that carry blood away
from the heart. Blood carried by arteries is usually highly oxygenated, having
just left the lungs on its way to the body’s tissues. The pulmonary trunk and
arteries of the pulmonary circulation loop provide an exception to this rule –
these arteries carry deoxygenated blood from the heart to the lungs to be
oxygenated.
Arteries face high levels of blood pressure as they carry blood being
pushed from the heart under great force. To withstand this pressure, the walls
of the arteries are thicker, more elastic, and more muscular than those of
other vessels. The largest arteries of the body contain a high percentage of
elastic tissue that allows them to stretch and accommodate the pressure of the
heart.
Smaller arteries are more muscular in the structure of their walls.
The smooth muscles of the arterial walls of these smaller arteries contract or
expand to regulate the flow of blood through their lumen. In this way, the body
controls how much blood flows to different parts of the body under varying
circumstances. The regulation of blood flow also affects blood pressure, as
smaller arteries give blood less area to flow through and therefore increases
the pressure of the blood on arterial walls.
Arterioles are narrower arteries that branch off from the ends of
arteries and carry blood to capillaries. They face much lower blood pressures
than arteries due to their greater number, decreased blood volume, and distance
from the direct pressure of the heart. Thus arteriole walls are much thinner
than those of arteries. Arterioles, like arteries, are able to use smooth
muscle to control their aperture and regulate blood flow and blood pressure.
Capillaries: Capillaries are the smallest and thinnest of the blood
vessels in the body and also the most common. They can be found running
throughout almost every tissue of the body and border the edges of the body’s
avascular tissues. Capillaries connect to arterioles on one end and venules on
the other.
Capillaries carry blood very close to the cells of the tissues of the
body in order to exchange gases, nutrients, and waste products. The walls of
capillaries consist of only a thin layer of endothelium so that there is the
minimum amount of structure possible between the blood and the tissues. The
endothelium acts as a filter to keep blood cells inside of the vessels while
allowing liquids, dissolved gases, and other chemicals to diffuse along their
concentration gradients into or out of tissues.
Precapillary sphincters are bands of smooth muscle found at the
arteriole ends of capillaries. These sphincters regulate blood flow into the
capillaries. Since there is a limited supply of blood, and not all tissues have
the same energy and oxygen requirements, the precapillary sphincters reduce
blood flow to inactive tissues and allow free flow into active tissues.
Veins and Venules: Veins are the large return vessels of the body and
act as the blood return counterparts of arteries. Because the arteries,
arterioles, and capillaries absorb most of the force of the heart’s
contractions, veins and venules are subjected to very low blood pressures. This
lack of pressure allows the walls of veins to be much thinner, less elastic,
and less muscular than the walls of arteries.
Veins rely on gravity, inertia, and the force of skeletal muscle
contractions to help push blood back to the heart. To facilitate the movement
of blood, some veins contain many one-way valves that prevent blood from
flowing away from the heart. As skeletal muscles in the body contract, they
squeeze nearby veins and push blood through valves closer to the heart.
When the muscle relaxes, the valve traps the blood until another
contraction pushes the blood closer to the heart. Venules are similar to
arterioles as they are small vessels that connect capillaries, but unlike
arterioles, venules connect to veins instead of arteries. Venules pick up blood
from many capillaries and deposit it into larger veins for transport back to
the heart.
Coronary Circulation
The heart has its own set of blood vessels that provide the myocardium with
the oxygen and nutrients necessary to pump blood throughout the body. The left
and right coronary arteries branch off from the aorta and provide blood to the
left and right sides of the heart. The coronary sinus is a vein on the
posterior side of the heart that returns deoxygenated blood from the myocardium
to the vena cava.
Hepatic Portal Circulation
The veins of the stomach and intestines perform a unique function: instead of
carrying blood directly back to the heart, they carry blood to the liver
through the hepatic portal vein. Blood leaving the digestive organs is rich in
nutrients and other chemicals absorbed from food. The liver removes toxins,
stores sugars, and processes the products of digestion before they reach the
other body tissues. Blood from the liver then returns to the heart through the
inferior vena cava.
Blood
The average human body contains about 4 to 5 liters of blood. As a liquid
connective tissue, it transports many substances through the body and helps to
maintain homeostasis of nutrients, wastes, and gases. Blood is made up of red
blood cells, white blood cells, platelets, and liquid plasma.
Red Blood Cells: Red blood cells, also known as erythrocytes, are by far
the most common type of blood cell and make up about 45% of blood volume.
Erythrocytes are produced inside of red bone marrow from stem cells at the
astonishing rate of about 2 million cells every second. The shape of
erythrocytes is biconcave—disks with a concave curve on both sides of the disk
so that the center of an erythrocyte is its thinnest part. The unique shape of
erythrocytes gives these cells a high surface area to volume ratio and allows
them to fold to fit into thin capillaries. Immature erythrocytes have a nucleus
that is ejected from the cell when it reaches maturity to provide it with its
unique shape and flexibility. The lack of a nucleus means that red blood cells
contain no DNA and are not able to repair themselves once damaged.
Erythrocytes transport oxygen in the blood through the red pigment
hemoglobin. Hemoglobin contains iron and proteins joined to greatly increase
the oxygen carrying capacity of erythrocytes. The high surface area to volume
ratio of erythrocytes allows oxygen to be easily transferred into the cell in
the lungs and out of the cell in the capillaries of the systemic tissues.
White Blood Cells: White blood cells, also known as leukocytes, make up a
very small percentage of the total number of cells in the bloodstream, but have
important functions in the body’s immune system. There are two major classes of
white blood cells: granular leukocytes and agranular leukocytes.
Granular Leukocytes: The three types of granular leukocytes are
neutrophils, eosinophils, and basophils. Each type of granular leukocyte is
classified by the presence of chemical-filled vesicles in their cytoplasm that
give them their function. Neutrophils contain digestive enzymes that neutralize
bacteria that invade the body. Eosinophils contain digestive enzymes
specialized for digesting viruses that have been bound to by antibodies in the
blood. Basophils release histamine to intensify allergic reactions and help
protect the body from parasites.
Agranular Leukocytes: The two major classes of agranular leukocytes are
lymphocytes and monocytes. Lymphocytes include T cells and natural killer cells
that fight off viral infections and B cells that produce antibodies against
infections by pathogens. Monocytes develop into cells called macrophages that
engulf and ingest pathogens and the dead cells from wounds or infections.
Platelets : Also known
as thrombocytes, platelets are small cell fragments responsible for the
clotting of blood and the formation of scabs. Platelets form in the red bone
marrow from large megakaryocyte cells that periodically rupture and release
thousands of pieces of membrane that become the platelets. Platelets do not
contain a nucleus and only survive in the body for up to a week before
macrophages capture and digest them.
Plasma: Plasma is the non-cellular or liquid portion of the blood that
makes up about 55% of the blood’s volume. Plasma is a mixture of water,
proteins, and dissolved substances. Around 90% of plasma is made of water,
although the exact percentage varies depending upon the hydration levels of the
individual. The proteins within plasma include antibodies and albumins.
Antibodies are part of the immune system and bind to antigens on the surface of
pathogens that infect the body. Albumins help maintain the body’s osmotic
balance by providing an isotonic solution for the cells of the body. Many
different substances can be found dissolved in the plasma, including glucose,
oxygen, carbon dioxide, electrolytes, nutrients, and cellular waste products. The
plasma functions as a transportation medium for these
substances as they move throughout the body.
Cardiovascular System Physiology
Functions of the Cardiovascular System
The cardiovascular system has three major functions: transportation of
materials, protection from pathogens, and regulation of the body’s homeostasis.
Transportation: The cardiovascular system transports blood to almost all of
the body’s tissues. The blood delivers essential nutrients and oxygen and
removes wastes and carbon dioxide to be processed or removed from the body.
Hormones are transported throughout the body via the blood’s liquid plasma.
Protection: The cardiovascular system protects the body through its white
blood cells. White blood cells clean up cellular debris and fight pathogens
that have entered the body. Platelets and red blood cells form scabs to seal
wounds and prevent pathogens from entering the body and liquids from leaking
out. Blood also carries antibodies that provide specific immunity to pathogens
that the body has previously been exposed to or has been vaccinated against.
Regulation: The cardiovascular system is instrumental in the body’s ability
to maintain homeostatic control of several internal conditions. Blood vessels
help maintain a stable body temperature by controlling the blood flow to the
surface of the skin. Blood vessels near the skin’s surface open during times of
overheating to allow hot blood to dump its heat into the body’s surroundings.
In the case of hypothermia, these blood vessels constrict to keep blood flowing
only to vital organs in the body’s core. Blood also helps balance the body’s pH
due to the presence of bicarbonate ions, which act as a buffer solution.
Finally, the albumins in blood plasma help to balance the osmotic concentration
of the body’s cells by maintaining an isotonic environment.
The Circulatory Pump
The heart is a four-chambered “double pump,” where each side (left and
right) operates as a separate pump. The left and right sides of the heart are
separated by a muscular wall of tissue known as the septum of the heart. The
right side of the heart receives deoxygenated blood from the systemic veins and
pumps it to the lungs for oxygenation. The left side of the heart receives
oxygenated blood from the lungs and pumps it through the systemic arteries to
the tissues of the body. Each heartbeat results in the simultaneous pumping of
both sides of the heart, making the heart a very efficient pump.
Regulation of Blood Pressure
Several functions of the cardiovascular system can control blood pressure.
Certain hormones along with autonomic nerve signals from the brain affect the
rate and strength of heart contractions. Greater contractile force and heart
rate lead to an increase in blood pressure. Blood vessels can also affect blood
pressure. Vasoconstriction decreases the diameter of an artery by contracting
the smooth muscle in the arterial wall. The sympathetic (fight or flight)
division of the autonomic nervous system causes vasoconstriction, which leads
to increases in blood pressure and decreases in blood flow in the constricted
region. Vasodilation is the expansion of an artery as the smooth muscle in the
arterial wall relaxes after the fight-or-flight response wears off or under the
effect of certain hormones or chemicals in the blood. The volume of blood in
the body also affects blood pressure. A higher volume of blood in the body
raises blood pressure by increasing the amount of blood pumped by each
heartbeat. Thicker, more viscous blood from clotting disorders can also raise
blood pressure.
Hemostasis
Hemostasis, or the clotting of blood and formation of scabs, is managed by
the platelets of the blood. Platelets normally remain inactive in the blood
until they reach damaged tissue or leak out of the blood vessels through a
wound. Once active, platelets change into a spiny ball shape and become very
sticky in order to latch on to damaged tissues. Platelets next release chemical
clotting factors and begin to produce the protein
fibrin to act as structure for the blood clot. Platelets also begin sticking
together to form a platelet plug. The platelet plug will serve as a temporary
seal to keep blood in the vessel and foreign material out of the vessel until
the cells of the blood vessel can repair the damage to the vessel wall.
Cardiovascular disease is a class of diseases that involve the heart or
blood vessels (arteries, capillaries and veins).
Cardiovascular disease refers to any disease that affects the
cardiovascular system, principally cardiac disease, vascular diseases of the
brain and kidney, and peripheral arterial disease. The causes of cardiovascular
disease are diverse but atherosclerosis and/or hypertension are the most
common. Besides, with aging come a number of physiological and morphological
changes that alter cardiovascular function and lead to
subsequently increased risk of cardiovascular disease, even in healthy
asymptomatic individuals.
Cardiovascular diseases remain the biggest cause of deaths worldwide,
though over the last two decades,[when?] cardiovascular
mortality rates have declined in many high-income countries. At the same time,
cardiovascular deaths and disease have increased at a fast rate in low- and
middle-income countries. Although cardiovascular disease usually affects older
adults, the antecedents of cardiovascular disease, notably atherosclerosis,
begin in early life, making primary prevention efforts necessary from
childhood. There is therefore increased emphasis on preventing atherosclerosis
by modifying risk factors, such as healthy eating, exercise, and avoidance of
smoking.
Micrograph of a heart with fibrosis (yellow) and amyloidosis (brown). Movat's stain
Types
Coronary heart disease (also ischaemic heart disease or coronary artery
disease). Coronary heart disease (CHD)
is the narrowing or blockage of the coronary arteries, usually caused by
atherosclerosis. Atherosclerosis (sometimes called “hardening” or “clogging” of
the arteries) is the buildup of cholesterol and fatty deposits (called plaques)
on the inner walls of the arteries. These plaques can restrict blood flow to
the heart muscle by physically clogging the artery or by causing abnormal
artery tone and function.
Without an adequate blood supply, the heart becomes starved of oxygen and
the vital nutrients it needs to work properly. This can cause chest pain called
angina. If blood supply to a portion of the heart muscle is cut off entirely,
or if the energy demands of the heart become much greater than its blood
supply, a heart attack (injury to the heart muscle) may occur.
It is most commonly equated with atherosclerotic coronary artery
disease, but coronary disease can be due to other causes, such as coronary
vasospasm, where the stenosis to be caused by spasm of the blood vessels of the
heart it is then usually called Prinzmetal's angina. Coronary artery disease
has a number of well determined risk factors. The most common risk factors
include smoking, family history, hypertension, obesity, diabetes, high alcohol
consumption, lack of exercise, stress, and hyperlipidemia Smoking appears to be
the cause for about 54% of cases and obesity 20%. Lack of exercise has been
linked to 7-12% of cases.
Job stress appear to play a minor role
accounting for about 3% of cases. In one study, women who were free of stress
from work life saw an increase in the diameter of their blood vessels, leading
to atherosclerosis. Contrastingly, women who had high levels of work-related
stress experienced a decrease in the diameter of their blood vessels. Also,
having a type A behavior pattern, a group of personality characteristics
including time urgency, competitiveness, hostility, and impatience is linked to an increased risk of coronary disease.
Parental history of high blood pressure can also contribute to a
higher risk of heart disease in an individual. People whose parents are
hypertensive have greater systolic and diastolic blood pressure numbers when
compared with individuals without hypertensive parents. High blood pressure has
been shown to be a cause of heart disease.
Treatment
Lifestyle
Lifestyle changes have been shown to be effective in reducing (and in
the case of diet, reversing) coronary disease:
A plant-based diet has been shown by Caldwell Esselstyn and T. Colin
Campbell among others to be effective as a treatment of coronary disease, and
generalized atherosclerosis. In several peer reviewed studies by Caldwell
Esselstyn the progression of heart disease has been shown to halt, and in some
cases, the disease process may be reversed. Information recommending a
healthier diet has been established for over 50 years.
Weight control
Smoking cessation
Avoiding the consumption of trans fats (in
partially hydrogenated oils)
Exercise Aerobic exercise, like walking, jogging, or swimming, can help
decrease blood pressure and the amount of blood cholesterol over time.
Fish oil consumption to increase omega-3 fatty acid intake
Decrease psychosocial stress.
Medications
Cholesterol lowering medications, such as statins, are useful to decrease
the amount of "bad" (LDL) cholesterol.
Nitroglycerin
ACE inhibitors, which treat hypertension and may lower the risk of
recurrent myocardial infarction
Calcium channel blockers and/or beta-blockers
Aspirin
Surgery
Coronary artery bypass
Heart transplant
Non-surgical
Coronary angioplasty (using stents).
Cardiomyopathy - diseases of cardiac muscle. Cardiomyopathy (literally
"heart muscle disease") is the measurable deterioration of the
function of the myocardium (the heart muscle) for any reason, usually leading
to heart failure; common symptoms are dyspnea (breathlessness) and peripheral
edema (swelling of the legs). People with cardiomyopathy are often at risk of
dangerous forms of irregular heart beat and sudden cardiac death. The most
common form of cardiomyopathy is dilated cardiomyopathy. Classification
Although in theory the term "cardiomyopathy" could apply to
almost any disease affecting the heart, in practice it is usually reserved for
"severe myocardial disease leading to heart failure".
Cardiomyopathies can be categorized as extrinsic or intrinsic.
An extrinsic cardiomyopathy is a cardiomyopathy where the primary pathology
is outside the myocardium itself. Most cardiomyopathies are extrinsic,
by far the most common cause of an extrinsic cardiomyopathy is ischemia.
Ischemia can be understood as poor oxygen supply of the heart muscle (the
demand for oxygen is higher than the current supply). The World Health
Organization calls these specific cardiomyopathies:
An intrinsic cardiomyopathy is defined as weakness in the muscle of the
heart not due to an identifiable external cause. This definition was used to
categorize previously idiopathic cardiomyopathies although specific external
causes have since been identified for many. For example, alcoholism has been
identified as a cause for some forms of dilated cardiomyopathy. To make a
diagnosis of an intrinsic cardiomyopathy, significant coronary artery disease
should be ruled out first (amongst other causes). The term intrinsic
cardiomyopathy does not describe the specific etiology of weakened heart
muscle. The intrinsic cardiomyopathies consist of a variety of disease states,
each with their own causes. Many intrinsic cardiomyopathies now have
identifiable external causes including drug and alcohol toxicity, certain
infections (including Hepatitis C), and various genetic and idiopathic (i.e.,
unknown) causes.
It is also possible to classify cardiomyopathies functionally, as
involving dilation, hypertrophy, or restriction.[6
Signs and symptoms This article needs additional citations
for verification. Please help improve this article by adding citations to
reliable sources. Unsourced material may be challenged and removed. (April
2012)
Symptoms and signs may mimic those of almost any form of heart
disease. Chest pain is common. Mild myocarditis or cardiomyopathy is frequently
asymptomatic; severe cases are associated with heart failure, arrhythmias, and
systemic embolization. Manifestations of the underlying disease (e.g., Chagas'
disease) may be prominent. Most patients with biopsy-proven myocarditis report
a recent viral prodrome preceding cardiovascular symptoms.
EKG abnormalities are often present, although the changes are
frequently nonspecific. A pattern characteristic of left ventricular
hypertrophy may be present. Flat or inverted T waves are most common, often
with low-voltage QRS complexes. Intraventricular conduction defects and bundle
branch block, especially left bundle branch block, are also common. An
echocardiogram is useful to detect wall motion abnormalities or a pericardial effusion.
Chest radiographs can be normal or can show evidence of congestive heart
failure with pulmonary edema or cardiomegaly.
Treatment
Treatment depends on the type of cardiomyopathy and condition of disease,
but may include medication (conservative treatment) or iatrogenic/implanted
pacemakers for slow heart rates, defibrillators for those prone to fatal heart
rhythms, ventricular assist devices (LVADs) for severe heart failure, or
ablation for recurring dysrhythmias that cannot be eliminated by medication or
cardioversion. The goal of treatment is often symptom relief, and some patients
may eventually require a heart transplant. Treatment of cardiomyopathy (and
other heart diseases) using alternative methods such as stem cell therapy is
commercially available but is not supported by convincing evidence.
Hypertensive heart disease - diseases of the heart secondary to high blood
pressure. Hypertensive heart disease
includes a number of complications of systemic arterial hypertension or high
blood pressure that affect the heart. While there are several definitions of
hypertensive heart disease in the medical literature, the term is most widely
used in the context of the International Classification of Diseases (ICD)
coding categories. The definition in the Tenth Revision of the International
Classification of Diseases (ICD-10) includes heart failure and other cardiac
complications of hypertension when a causal relationship between the heart
disease and hypertension is stated or implied on the death certificate. According to ICD-10, hypertensive heart disease (I11), and its
subcategories: hypertensive heart disease with heart failure (I11.0) and
hypertensive heart disease without heart failure (I11.9) are distinguished from
chronic rheumatic heart diseases (I05-I09), other forms of heart disease
(I30-I52) and ischemic heart diseases (I20-I25). However, since high
blood pressure is a risk factor for atherosclerosis and ischemic heart disease,
death rates from hypertensive heart disease provide an incomplete measure of
the burden of disease due to high blood pressure.
Symptoms and signs
The symptoms and signs of hypertensive heart disease will depend on whether
or not it is accompanied by heart failure. In the absence of heart failure,
hypertension, with or without enlargement of the heart (left ventricular
hypertrophy) is usually symptomless. Symptoms and signs of chronic heart
failure can include:
1.
Fatigue
2.
Irregular pulse or palpitations
3.
Swelling of feet and ankles
4.
Weight gain
5.
Nausea
6.
Shortness of breath
7. Difficulty sleeping
flat in bed (orthopnea)
8. Bloating and
abdominal pain
9. Greater need to
urinate at night
10. Altered
mentation (in severe cases)
11. An enlarged
heart (cardiomegaly)
Patients can present acutely with heart failure and pulmonary edema due to
sudden failure of pump function of the heart. Acute heart failure can be
precipitated by a variety of causes including myocardial ischemia, marked increases
in blood pressure, or cardiac dysrhythmias, especially atrial fibrillation.
Alternatively heart failure can develop insidiously over time.
Associated conditions (potential complications)
Left ventricular hypertrophy and left ventricular remodeling
Diminished coronary flow reserve and silent myocardial ischemia
Coronary heart disease and accelerated atherosclerosis
Congestive heart failure, including Heart Failure With
Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart
failure
Atrial fibrillation, other cardiac arrhythmias and sudden cardiac death
Differential diagnosis
Other conditions can share features with hypertensive heart disease and
need to be considered in the differential diagnosis. For example:
Coronary artery disease or ischemic heart disease due to atherosclerosis
Hypertrophic cardiomyopathy
Left ventricular hypertrophy in athletes
Congestive heart failure or heart failure with normal ejection fraction due
to other causes
Atrial fibrillation or other disorders of cardiac rhythm due to other
causes
Sleep apnea
Treatment
Treatment of hypertensive heart disease aims to normalize the elevated
blood pressure and prevent and/or treat the cardiac consequences of
hypertension. The risk of cardiovascular disease and death can be reduced by
lifestyle modifications, including dietary advice, promotion of weight loss and
regular aerobic exercise, moderation of alcohol intake and cessation of
smoking. Drug treatment may also be needed to control the hypertension and
reduce the risk of cardiovascular disease, manage the heart failure, or control
cardiac arrhythmias. Patients with hypertensive heart disease should avoid
taking over the counter non-steroidal anti-inflammatory drugs (NSAIDs), or
cough suppressants, and decongestants containing sympathomimetics, unless
otherwise advised by their physician as these can exacerbate hypertension and
heart failure.
Heart failure. Heart
failure (HF), often called congestive heart failure (CHF) or congestive cardiac
failure (CCF), occurs when the heart is unable to
provide sufficient pump action to distribute blood flow to meet the needs of
the body. Heart failure can cause a number of symptoms including shortness of
breath, leg swelling, and exercise intolerance. The condition is diagnosed with
echocardiography and blood tests. Treatment commonly consists of lifestyle
measures such as smoking cessation, light exercise including breathing
protocols, decreased salt intake and other dietary changes, and medications.
Sometimes it is treated with implanted devices (pacemakers or ventricular
assist devices) and occasionally a heart transplant.
Common causes of heart failure include myocardial infarction and other
forms of ischemic heart disease, hypertension, valvular heart disease, and
cardiomyopathy. The term heart failure is sometimes incorrectly used for other
cardiac-related illnesses, such as myocardial infarction (heart attack) or
cardiac arrest, which can cause heart failure but are not equivalent to heart
failure.
Heart failure is a common, costly, disabling, and potentially deadly
condition. In developed countries, around 2% of adults suffer from heart
failure, but in those over the age of 65, this increases to 6–10%.
The major signs and symptoms of heart failure
Cor pulmonale - a failure of the right side of the heart. Cor pulmonale (Latin cor, heart + New Latin pulmōnāle, of the
lungs) or pulmonary heart disease is enlargement of the right ventricle of the
heart as a response to increased resistance or high blood pressure in the lungs
(pulmonary hypertension).
Chronic cor pulmonale usually results in right ventricular
hypertrophy (RVH), whereas acute cor pulmonale usually results in dilatation.
Hypertrophy is an adaptive response to a long-term increase in pressure.
Individual muscle cells grow larger (in thickness) and change to drive the
increased contractile force required to move the blood against greater
resistance.
Dilatation is a stretching (in length) of the ventricle in response
to acute increased pressure, such as when caused by a pulmonary embolism.
To be classified as cor pulmonale, the cause must originate in the
pulmonary circulation system. Two major causes are vascular changes as a result
of tissue damage (e.g. disease, hypoxic injury, chemical agents, etc.), and
chronic hypoxic pulmonary vasoconstriction. RVH due to a systemic defect is not
classified as cor pulmonale.
If left untreated, cor pulmonale can lead to right-heart failure and
death. Symptoms
The symptoms of pulmonary heart disease depend on the stage of the
disorder. In the early stages, one may have no symptoms but as pulmonary heart
disease progresses, most individuals will develop the symptoms like:
Shortness of breath which occurs on exertion but when severe can occur at
rest
·
Wheezing
·
Chronic wet cough
·
Swelling of the abdomen with fluid (ascites)
·
Swelling of the ankles and feet (pedal edema)
·
Enlargement or prominent neck and facial veins
·
Raised Jugular Venous Pulse (JVP)
·
Enlargement of the liver
·
Bluish discoloration of face
·
Presence of abnormal heart sounds
·
possible bi-phasic atrial response shown on an EKG due
to hypertrophy
Diagnosis
In many cases, the diagnosis of pulmonary heart disease is not easy as both
the lung and heart disease can produce similar symptoms. Most patients undergo
an ECG, chest X ray, echocardiogram, CT scan of the chest and a cardiac
catheterization. During a cardiac catheterization, a small flexible tube is
inserted from the groin and under x ray guidance
images of the heart are obtained. Moreover the technique allows measurement of
pressures in the lung and heart which provide a clue to the diagnosis.
Treatment
Elimination of the cause is the most important intervention. Smoking must
be stopped, exposure to dust, flames, household smoke
and to cold weather is avoided. If there is evidence of respiratory infection,
it should be treated with appropriate antibiotics after culture and
sensitivity. Diuretics for RVF, In pulmonary embolism,
thrombolysis (enzymatic dissolution of the blood clot) is advocated by some
authorities if there is dysfunction of the right ventricle, and is otherwise
treated with anticoagulants. In COPD, long-term oxygen therapy may improve cor
pulmonale.
Cor pulmonale may lead to congestive heart failure (CHF), with
worsening of respiration due to pulmonary edema, swelling of the legs due to
peripheral edema and painful congestive hepatomegaly (enlargement of the liver
due to tissue damage as explained in the Complications section. This situation
requires diuretics (to decrease strain on the heart), sometimes nitrates (to
improve blood flow), phosphodiesterase inhibitors such as sildenafil or
tadalafil and occasionally inotropes (to improve heart contractility). CHF is a
negative prognostic indicator in cor pulmonale.
Oxygen is often required to resolve the shortness of breath. Plus,
oxygen to the lungs also helps relax the blood vessels and eases right heart
failure. Oxygen is given at the rate of 2 litres per minute. Excess oxygen can
be harmful to patients because hypoxia is the main stimulus to respiration. If
such hypoxia is suddenly corrected by overflow of oxygen, such stimulus to the
respiratory center is suddenly withdrawn and respiratory arrest occurs. When
wheezing is present, majority of the patients require bronchodilators. A
variety of drugs have been developed to relax the blood vessels in the lung.
Calcium channel blockers are used but only work in a few cases. Other novel
medications that need to be inhaled or given intravenously include prostacyclin
derivatives.
Cases of COPD with chronic corpulmonale present with secondary
polycythemia, if severe it may increase the blood viscosity and contribute to
pulmonary hypertension. If hematocrit(PCV) is above
60%, then it is better to reduce the red blood cell count by phlebotomies.
Mucolytic agents like bromhexine and carbocisteine help bring out
excessive bronchial secretions more easily by coughing.
All patients with pulmonary heart disease are maintained on blood
thinning medications to prevent formation of blood clots.
When medical therapy fails, one may require a transplant. However,
since the lungs are damaged, both the heart and lungs needs to be transplanted.
With a shortage of donors this therapy is only done 10-15 times a year in North
America.
Prevention
While not all lung diseases can be prevented one can reduce the risk of
lung disease. This means avoiding or discontinuing smoking. Patients with end
stage emphysema or chronic obstructive lung disease always end up with right
heart failure. When working in environments where there are chemicals, wear
masks to prevent inhalation of dust particles.
Cardiac dysrhythmias - abnormalities of heart rhythm. Cardiac dysrhythmia (also known as arrhythmia or irregular heartbeat) is
any of a large and heterogeneous group of conditions in which there is abnormal
electrical activity in the heart. The heartbeat may be too fast or too slow,
and may be regular or irregular. A heart beat that is too fast is called
tachycardia and a heart beat that is too slow is called bradycardia.
Some arrhythmias are life-threatening medical emergencies that can
result in cardiac arrest. In fact, cardiac arrythmias are one of the most
common causes of death when travelling to a hospital. Others cause symptoms
such as an abnormal awareness of heart beat (palpitations), and may be merely
uncomfortable. These palpitations have also been known to be caused by
atrial/ventricular fibrillation, wire faults, and other technical or mechanical
issues in cardiac pacemakers/defibrillators. Still others may not be associated
with any symptoms at all, but may predispose the patient to potentially life
threatening stroke or embolism.
The term sinus arrhythmia refers to a normal phenomenon of mild
acceleration and slowing of the heart rate that occurs with breathing in and
out. It is usually quite pronounced in children, and steadily decreases with
age. This can also be present during meditation breathing exercises that
involve deep inhaling and breath holding patterns. Proarrhythmia is a new or
more frequent occurrence of pre-existing arrhythmias, paradoxically
precipitated by antiarrhythmic therapy, which means it is a side effect
associated with the administration of some existing antiarrhythmic drugs, as
well as drugs for other indications. In other words, it is a tendency of
antiarrhythmic drugs to facilitate emergence of new arrhythmias. Some
arrhythmias are very minor and can be regarded as normal variants. In fact,
most people will on occasion feel their heart skip a beat, or give an
occasional extra strong beat; neither of these is usually a cause for alarm.
Classification
Arrhythmia may be classified by rate (normal sinus rhythm,
tachycardia, bradycardia), or mechanism (automaticity, reentry, junctional,
fibrillation).
It is also appropriate to classify by site of origin:
·
Atrial
·
Premature Atrial Contractions (PACs)
·
Wandering Atrial Pacemaker
·
Multifocal atrial tachycardia
·
Atrial flutter
·
Atrial fibrillation (Afib)
·
[edit]
·
Junctional arrhythmias
·
Supraventricular tachycardia (SVT)
·
AV nodal reentrant tachycardia is the most common cause of Paroxysmal
Supra-ventricular Tachycardia (PSVT)
·
Junctional rhythm
·
Junctional tachycardia
·
Premature junctional contraction
Ventricular
Premature Ventricular Contractions (PVC) sometimes called Ventricular Extra
Beats (VEBs)
Premature Ventricular beats occurring after every normal beat are termed
"ventricular bigeminy"
PVCs that occur at intervals of 2 normal beats to 1 PVC
are termed "PVCs in trigeminy"
Three premature ventricular grouped together is termed a "run of
PVCs"; runs lasting longer than three beats are generally referred to as
ventricular tachycardia
Accelerated idioventricular rhythm
Monomorphic Ventricular tachycardia
Polymorphic ventricular tachycardia
Ventricular fibrillation
Heart blocks
These are also known as AV blocks, because the vast majority of them arise
from pathology at the atrioventricular node. They are the most common causes of
bradycardia:
First degree heart block, which manifests as PR prolongation
Second degree heart block
Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
Type 2 Second degree heart block, also known as Mobitz II
Third degree heart block, also known as complete heart block.
SADS
SADS, or sudden arrhythmic death syndrome, is a term (as part of , Sudden
unexpected death syndrome) used to describe sudden death due to cardiac arrest
brought on by an arrhythmia in the absence of any structural heart disease on
autopsy. The most common cause of sudden death in the US is coronary artery
disease.[citation needed] Approximately 180,000 to
250,000 people die suddenly of this cause every year in the US. SADS occurs
from other causes. There are many inherited conditions and heart diseases that
can affect young people and subsequently cause sudden death. Many of these
victims have no symptoms before dying suddenly.
Causes of SADS in young people include viral myocarditis, long QT
syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular
tachycardia, hypertrophic cardiomyopathy and arrhythmogenic right ventricular
dysplasia.
Signs and symptoms
The term cardiac arrhythmia covers a very large number of very different
conditions.
The most common symptom of arrhythmia is an abnormal awareness of
heartbeat, called palpitations. These may be infrequent, frequent, or
continuous. Some of these arrhythmias are harmless (though distracting for
patients) but many of them predispose to adverse outcomes.
Some arrhythmias do not cause symptoms, and are not associated with
increased mortality. However, some asymptomatic arrhythmias are associated with
adverse events. Examples include a higher risk of blood clotting within the
heart and a higher risk of insufficient blood being transported to the heart
because of weak heartbeat. Other increased risks are of embolisation and
stroke, heart failure and sudden cardiac death.
If an arrhythmia results in a heartbeat that is too fast, too slow or
too weak to supply the body's needs, this manifests as a lower blood pressure
and may cause lightheadedness or dizziness, or syncope (fainting).
Some types of arrhythmia result in cardiac arrest, or sudden death.
Medical assessment of the abnormality using an electrocardiogram is
one way to diagnose and assess the risk of any given arrhythmia.
Differential diagnosis
Normal electrical activity
Each heart beat originates as an electrical impulse from a small area
of tissue in the right atrium of the heart called the sinus node or Sino-atrial
node or SA node. The impulse initially causes both atria to contract, then
activates the atrioventricular (or AV) node which is normally the only
electrical connection between the atria and the ventricles (main pumping
chambers). The impulse then spreads through both ventricles via the Bundle of
His and the Purkinje fibres causing a synchronised contraction of the heart muscle
and, thus, the pulse.
In adults the normal resting heart rate ranges from 60 to 80 beats
per minute. The resting heart rate in children is much faster. In athletes
though, the resting heart rate can be as slow as 40 beats per minute, and be
considered as normal.
Bradycardias
Normal sinus rhythm, with solid black arrows pointing to normal P
waves representative of normal sinus node function, followed by a pause in
sinus node activity (resulting in a transient loss of heart beats). Note that
the P wave that disrupts the pause (indicated by the dashed arrow) does not
look like the previous (normal) P waves — this last P wave is arising from a
different part of the atrium, representing an escape rhythm.
A slow rhythm (less than 60 beats/min), is labelled bradycardia. This may
be caused by a slowed signal from the sinus node (sinus bradycardia), a pause
in the normal activity of the sinus node (sinus arrest), or by blocking of the
electrical impulse on its way from the atria to the ventricles (AV block or
heart block). Heart block comes in varying degrees and severity. It may be
caused by reversible poisoning of the AV node (with drugs that impair
conduction) or by irreversible damage to the node. Bradycardias may also be
present in the normally functioning heart of endurance athletes or other
well-conditioned persons.
Tachycardias
In adults and children over 15, resting heart rate faster than 100 beats/minute is labelled tachycardia. Tachycardia may
result in palpitation; however, tachycardia is not necessarily an arrhythmia.
Increased heart rate is a normal response to physical exercise or emotional
stress. This is mediated by the sympathetic nervous system on the sinus node
and called sinus tachycardia. Other things that increase sympathetic nervous system
activity in the heart include ingested or injected substances, such as caffeine
or amphetamines, and an overactive thyroid gland (hyperthyroidism).
Tachycardia that is not sinus tachycardia usually results from the
addition of abnormal impulses to the normal cardiac cycle. Abnormal impulses
can begin by one of three mechanisms: automaticity, reentry or triggered
activity. A specialised form of re-entry problem is termed fibrillation.
Heart Defects Causing Tachycardia Congenital heart defects are structural
or electrical pathway problems in the heart that are present at birth. Anyone
can be effected with this because overall health does
not play a role in the problem. Problems with the electrical pathway of the
heart can cause very fast or even deadly arrhythmias. Wolf-Parkinson-White
syndrome is due to an extra pathway in the heart that is made up of electrical
muscle tissue. This tissue allows the electrical impulse, which stimulates the
heartbeat, to happen very rapidly. Right Ventricular Outflow Tract Tachycardia
is the most common type of ventricular tachycardia in otherwise healthy
individuals. This defect is due to an electrical node in the right ventricle
just before the pulmonary artery. When the node is stimulated, the patient will
go into ventricular tachycardia, which does not allow the heart to fill with
blood before beating again. Long QT Syndrome is another complex problem in the
heart and has been labeled as an independent factor in mortality. There are
multiple methods of treatment for these including cardiac ablations, medication
treatment, or altering your lifestyle to have less stress and exercise. It is
possible to live a full and happy life with these conditions.
Automaticity
Automaticity refers to a cardiac muscle cell firing off an impulse on its
own. All of the cells in the heart have the ability to initiate an action
potential; however, only some of these cells are designed to routinely trigger
heart beats. These cells are found in the conduction system of the heart and include
the SA node, AV node, Bundle of His and Purkinje fibers. The sinoatrial node is
a single specialized location in the atrium which has a higher automaticity (a
faster pacemaker) than the rest of the heart and, therefore, is usually
responsible for setting the heart rate and initiating each heart beat.
Any part of the heart that initiates an impulse without waiting for
the sinoatrial node is called an ectopic focus and is, by definition, a
pathological phenomenon. This may cause a single premature beat now and then,
or, if the ectopic focus fires more often than the sinoatrial node, it can
produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in
the atria, or by the atrioventricular node, are the least dangerous
dysrhythmias; but they can still produce a decrease in the heart's pumping
efficiency, because the signal reaches the various parts of the heart muscle
with different timing than usual and can be responsible for poorly coordinated
contraction.
Conditions that increase automaticity include sympathetic nervous
system stimulation and hypoxia. The resulting heart rhythm depends on where the
first signal begins: If it is the sinoatrial node, the rhythm remains normal
but rapid; if it is an ectopic focus, many types of dysrhythmia may ensue.
Re-entry
Re-entry arrhythmias occur when an electrical impulse recurrently travels
in a tight circle within the heart, rather than moving from one end of the
heart to the other and then stopping. Every cardiac cell is able to transmit
impulses in every direction but will only do so once within a short time.
Normally, the action potential impulse will spread through the heart quickly
enough that each cell will only respond once. However, if conduction is
abnormally slow in some areas (for example in heart damage) so the myocardial
cells are unable to activate the fast sodium channel, part of the impulse will
arrive late and potentially be treated as a new impulse. Depending on the
timing, this can produce a sustained abnormal circuit rhythm. Re-entry circuits
are responsible for atrial flutter, most paroxysmal supraventricular
tachycardia, and dangerous ventricular tachycardia. These types of re-entry
circuits are different from WPW syndromes in which the real pathways existed.
Although omega-3 fatty acids from fish oil can be protective against
arrhythmias, in the case of re-entrant arrhythmias, fish oil can worsen the
arrhythmia.
Fibrillation
When an entire chamber of the heart is involved in a multiple micro-reentry
circuits and, therefore, quivering with chaotic electrical impulses, it is said
to be in fibrillation.
Fibrillation can affect the atrium (atrial fibrillation) or the
ventricle (ventricular fibrillation); ventricular fibrillation is imminently
life-threatening.
Atrial fibrillation affects the upper chambers of the heart, known as the
atria. Atrial fibrillation may be due to serious underlying medical conditions
and should be evaluated by a physician. It is not typically a medical
emergency.
Ventricular fibrillation occurs in the ventricles (lower chambers) of the
heart; it is always a medical emergency. If left untreated, ventricular
fibrillation (VF, or V-fib) can lead to death within
minutes. When a heart goes into V-fib, effective pumping of the blood stops.
V-fib is considered a form of cardiac arrest. An individual suffering from it
will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation
are provided immediately.
CPR can prolong the survival of the brain in the lack of a normal
pulse, but defibrillation is the only intervention that can restore a healthy
heart rhythm. Defibrillation is performed by applying an electric shock to the
heart, which resets the cells, permitting a normal beat to re-establish itself.
Triggered beats
Triggered beats occur when problems at the level of the ion channels in
individual heart cells result in abnormal propagation of electrical activity
and can lead to sustained abnormal rhythm. They are relatively rare and can
result from the action of anti-arrhythmic drugs. See early and delayed
Afterdepolarizations.
Diagnostic approach
Cardiac dysrhythmias are often first detected by simple but nonspecific
means: auscultation of the heartbeat with a stethoscope, or feeling for
peripheral pulses. These cannot usually diagnose specific dysrhythmias, but can
give a general indication of the heart rate and whether it is regular or
irregular. Not all the electrical impulses of the heart produce audible or
palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do
not produce an effective pumping action and are experienced as
"skipped" beats.
The simplest specific diagnostic test for assessment of heart rhythm
is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG
recorded over a 24-hour period, to detect dysrhythmias that may happen briefly
and unpredictably throughout the day.
A more advanced study of the heart's electrical activity can be
performed to assess the source of the aberrant heart beats. This can be
accomplished in an Electrophysiology study. A minimally invasive procedure that
uses a catheter to "listen" to the electrical activity from within
the heart, additionally if the source of the arrhythmias is found, often the
abnormal cells can be ablated and the arrhythmia can be permanently corrected.
Inflammatory heart disease
·
Endocarditis – inflammation of the inner layer of the heart, the endocardium.
The structures most commonly involved are the heart valves.
·
Inflammatory cardiomegaly
·
Myocarditis – inflammation of the myocardium, the muscular part of the heart.
·
Valvular heart disease
·
Stroke and cerebrovascular disease
·
Peripheral arterial disease
CIRCULATORY DISEASE CONDITIONS
The leading cause of untimely death in the Western countries of the world
is cardiovascular disease.
There are several hereditary factors that influence whether a person
will get cardiovascular disease:
1. family history of heart attack
2. gender (males are high risk)
3. race/ethnicity
(African Americans high risk)
Whether or not you have a hereditary factor, there are some things
you can do to prevent heart disease with diet and exercise. Included in
this is knowing your cholesterol level, lowering your LDL intake, use olive and
canola oil rather than butter/cream.
Some studies also suggest that antioxidant vitamins (A, E, and C) may help,
but remember that too much vitamin A and E cause a lot more harm to the liver
than good to the circulation.
1. ATHEROSCLEROSIS is fat and cholesterol
deposits underneath the lining of arteries.
When it builds up in a lump in one place, it is called a PLAQUE.
It causes the lumen to narrow, restricting blood flow. If this plaque
breaks off and travels in the bloodstream, it is now called an EMBOLISM.
In a coronary artery, it will cause ANGINA (heart pain).
If a platelet catches on a piece of this fat, it can start a blood clot. If a
piece of the clot breaks off and enters the circulation, it can lodge in a
smaller blood vessel and block the oxygen to all the tissue past that point, and the tissue dies.
If this occurs in the coronary arteries à myocardial infarct (Heart
attack).
If it occurs in an artery in the brain à stroke
2. ARTERIOSCLEROSIS is known as “hardening of the arteries”. It
is caused by calcium deposits in the artery walls. The blood vessel
becomes hard like a rock; it can’t expand or contract, causes increase in blood
pressure. Diet and exercise don’t help this much. Both arteriosclerosis
and atherosclerosis cause high blood pressure.
3. HYPERTENSION (High Blood Pressure)
High blood pressure is due to high pressure of blood against the walls of
the blood vessels; the blood vessels compensate by developing a thicker
wall. The vessels can no longer expand during systole, so the vessel gets
thicker and thicker, and the blood pressure goes up more. If the blood
pressure gets too high, an ANEURYSM can form, which is a weakening in
the wall of the blood vessel, causing it to expand like a balloon. If
it ruptures, it’s very dangerous. The aorta is the first artery that
leaves the heart. It is under high pressure, so it is susceptible to rupture;
you’ll be dead in three heart beats. Can also get
aneurysms in the brain that cause stroke. Aneurysms have no symptoms.
VARICOSE VEINS
An inflammation of the veins, usually due to lack of movement. One treatment of superficial varicose veins is stripping (removing)
the vein. Not a problem because there are so many. In the rectum, a
varicose vein is called a HEMORRHOID.
ARTIFICIAL HEART
An artificial heart is a device that replaces the heart. Artificial hearts
are typically used to bridge the time to heart transplantation, or to
permanently replace the heart in case heart transplantation is impossible.
Although other similar inventions preceded it going back to the late 1940s, the
first artificial heart to be successfully implanted in a human was the
Jarvik-7, designed by Robert Jarvik and implemented in 1982. The first two
patients to receive these hearts, Barney Clark and William Schroeder, survived
112 and 620 days beyond their surgeries, respectively.
An artificial heart is distinct from a ventricular assist device
designed to support a failing heart. It is also distinct from a cardiopulmonary
bypass machine, which is an external device used to provide the functions of
both the heart and lungs and are only used for a few hours at a time, most
commonly during cardiac surgery.
The SynCardia temporary Total Artificial Heart
An artificial heart displayed at the London Science Museum
FDA approved artificial hearts
SynCardia temporary Total Artificial Heart
Similar to a heart transplant, the SynCardia temporary Total Artificial
Heart replaces both failing heart ventricles and the four heart valves.
The SynCardia temporary Total Artificial Heart (formerly known as the
CardioWest TAH), manufactured by SynCardia Systems, Inc. was the first
FDA-approved total artificial heart. It received FDA approval on October 15,
2004, following a 10-year clinical study.
Originally designed as a permanent replacement heart, it is currently
approved as a bridge to donor heart transplant for patients dying because both
sides of their hearts are failing (irreversible, end-stage biventricular
failure). SynCardia claims there are more than 1000 implants of the Total
Artificial Heart, accounting for more than 270 patient years of life on this
device. During the 10-year pivotal clinical study, 79% of patients receiving
the Total Artificial Heart survived to transplant (New England Journal of
Medicine 2004; 351: 859–867). This is the highest bridge-to-transplant rate for
any heart device in the world.
In 2010, SynCardia's Freedom portable driver, the world's first wearable
power supply for the Total Artificial Heart, received the CE Mark for use in
Europe and FDA approval to undergo an Investigational Device Exemption (IDE)
clinical study in the U.S. Weighing 13.5 pounds (6.1 kilograms), the Freedom
driver allows stable Total Artificial Heart patients who meet discharge
criteria to leave the hospital and resume their lives at home and in their
communities while they wait for a matching donor heart. On April 24, 2012,
SynCardia completed the minimum enrollment required by the clinical study. The
company plans to submit the Freedom portable driver for FDA approval through a
post-market approval supplement in Q4 2012.
According to SynCardia, the longest a patient has been supported with
the Total Artificial Heart is 1,374 days (nearly four years) before he received
a successful heart transplant.
AbioCor Replacement Heart
Unlike the CardioWest TAH, the AbioCor Replacement Heart by AbioMed is
fully implantable, meaning that no wires or tubes penetrate the skin, and,
therefore, there is less risk of infection.
The AbioCor is approved for use in severe biventricular end-stage
heart disease patients who are not eligible for heart transplant and have no
other viable treatment options. As of April 2011, 14 patients have been
implanted with the AbioCor, with one patient living for 512 days with the
AbioCor.
The AbioCor received FDA approval under a Humanitarian Device
Exemption (HDE) on September 5, 2006. The first implant of the AbioCor since
receiving FDA approval in 2006 took place on June 24, 2009, at Robert Wood
Johnson University Hospital, New Brunswick, New Jersey. This patient later died
on August 23, 2009. (See FDA Summary of Safety and Probable Benefit.) Abiomed
is no longer actively marketing the AbioCor. In a November 2009 article in the
Boston Globe, Abiomed's CEO Mike Minogue said, "I consider this thing the
sports car you watch on television, but you can't buy from your dealer."
Origins
A synthetic replacement for the heart remains one of the long-sought holy
grails of modern medicine. The obvious benefit of a functional artificial heart
would be to lower the need for heart transplants, because the demand for organs
always greatly exceeds supply.
Although the heart is conceptually a pump, it embodies subtleties
that defy straightforward emulation with synthetic materials and power
supplies. Consequences of these issues include severe foreign-body rejection
and external batteries that limit patient mobility. These complications limited
the lifespan of early human recipients to hours or days.
Early development
A heart-lung machine was used in 1953 during a successful open heart
surgery. Dr. John Heysham Gibbon, the inventor of the machine, performed the
operation and developed the heart-lung substitute himself.
Although Jarvik created the idea and rough draft for the artificial
heart, his models were not created of a material that the human body would
accept. Dayton, Ohio's Ival O. Salyer, along with various colleagues, developed
a polymer material that the human body would not necessarily reject.
On July 3, 1952, 41-year-old Henry Opitek, suffering from shortness
of breath, made medical history at Harper University Hospital at Wayne State
University in Michigan. The Dodrill-GMR heart machine, considered to be the
first operational mechanical heart, was successfully used while performing
heart surgery.
Dr. Forest Dewey Dodrill used the machine in 1952 to bypass Henry
Opitek's left ventricle for 50 minutes while he opened the patient's left
atrium and worked to repair the mitral valve. In Dr. Dodrill's post-operative
report, he notes, "To our knowledge, this is the first instance of
survival of a patient when a mechanical heart mechanism was used to take over
the complete body function of maintaining the blood supply of the body while
the heart was open and operated on."
The scientific interest for the development of a solution for heart disease
developed in different research groups worldwide.
Early designs of total artificial hearts
In 1949, a precursor to the modern artificial heart pump was built by
doctors William Sewell and William Glenn of the Yale School of Medicine using
an Erector Set, assorted odds and ends, and dime-store toys. The external pump
successfully bypassed the heart of a dog for more than an hour.
American ventriloquist and inventor Paul Winchell invented an
artificial heart with the assistance of Dr. Henry Heimlich (the inventor of the
Heimlich Maneuver) and held the first patent for such
a device. The University of Utah developed a similar apparatus around the same
time, but when they tried to patent it, Winchell's heart was cited as prior
art. The university requested that Winchell donate the heart to the University
of Utah, which he did. There is some debate as to how much of Winchell's design
Dr. Robert Jarvik used in creating Jarvik's artificial heart. Dr. Heimlich
states, "I saw the heart, I saw the patent and I saw the letters. The
basic principle used in Winchell's heart and Jarvik's heart is exactly the
same." Jarvik denies that any of Winchell's design elements were
incorporated into the device he fabricated for humans which was successfully
implanted into Barney Clark in 1982.
On December 12, 1957, Dr. Willem Johan Kolff, the world's most
prolific inventor of artificial organs, implanted an artificial heart into a
dog at Cleveland Clinic. The dog lived for 90 minutes.
In 1958, Domingo Liotta initiated the studies of TAH replacement at
Lyon, France, and in 1959–60 at the National University of Córdoba, Argentina.
He presented his work at the meeting of the American Society for Artificial Internal
Organs held in Atlantic City in March 1961. At that meeting, Dr. Liotta
described the implantation of three types of orthotopic (inside the pericardial
sac) TAHs in dogs, each of which used a different source of external energy: an
implantable electric motor, an implantable rotating pump with an external
electric motor, and a pneumatic pump.
In 1964, the National Institutes of Health started the Artificial Heart
Program, with the goal of putting a man-made organ into a human by the end of
the decade.
In February 1966, Dr. Adrian Kantrowitz rose to international
prominence when he performed the world's first permanent implantation of a
partial mechanical heart (left ventricular assist device) at Maimonides Medical
Center.
In 1967, Dr. Kolff left Cleveland Clinic to start the Division of
Artificial Organs at the University of Utah and pursue his work on the
artificial heart.
In 1973, a calf named Tony survived for 30 days on an early Kolff heart.
In 1975, a bull named Burk survived 90 days on the artificial heart.
In 1976, a calf named Abebe lived for 184 days on the Jarvik 5 artificial
heart.
In 1981, a calf named Alfred Lord Tennyson lived for 268 days on the Jarvik
5.
Over the years, more than 200 physicians, engineers, students and
faculty developed, tested and improved Dr. Kolff's artificial heart. To help
manage his many endeavors, Dr. Kolff assigned project managers. Each project
was named after its manager. Graduate student Robert Jarvik was the project
manager for the artificial heart, which was subsequently renamed the Jarvik 7.
In 1981, Dr. William DeVries submitted a request to the FDA to
implant the Jarvik 7 into a human being. On December 2, 1982, Dr. Kolff
implanted the Jarvik 7 artificial heart into Barney Clark, a dentist from Seattle
who was suffering from severe congestive heart failure. While Clark lived for
112 days tethered to an external pneumatic compressor, a device weighing some
400 pounds (180 kg), during that time he suffered prolonged periods of
confusion and a number of instances of bleeding, and asked several times to be
allowed to die.
First clinical implantation of a total artificial heart
On April 4, 1969, Domingo Liotta and Denton A. Cooley replaced a dying
man's heart with a mechanical heart inside the chest at The Texas Heart
Institute in Houston as a bridge for a transplant. The patient woke up and
recovered well. After 64 hours, the pneumatic-powered artificial heart was
removed and replaced by a donor heart. However thirty-two hours after
transplantation, the patient died of what was later proved to be an acute
pulmonary infection, extended to both lungs, caused by fungi, most likely
caused by an immunosuppressive drug complication.
The original prototype of Liotta-Cooley artificial heart used in this
historic operation is prominently displayed in the Smithsonian Institution's
National Museum of American History "Treasures of American History"
exhibit in Washington, D.C.
First clinical applications of a permanent pneumatic total artificial
heart
The eighty-fifth clinical use of an artificial heart designed for permanent
implantation rather than a bridge to transplant occurred in 1982 at the
University of Utah. Artificial kidney pioneer Dr. Willem Johan Kolff started
the Utah artificial organs program in 1967. There, physician-engineer Dr.
Clifford Kwan-Gett invented two components of an integrated pneumatic
artificial heart system: a ventricle with hemispherical diaphragms that did not
crush red blood cells (a problem with previous artificial hearts) and an external
heart driver that inherently regulated blood flow without needing complex
control systems. Independently, ventriloquist Paul Winchell designed and
patented a similarly shaped ventricle and donated the patent to the Utah
program. Throughout the 1970s and early 1980s, veterinarian Dr. Donald Olsen
led a series of calf experiments that refined the artificial heart and its
surgical care. During that time, as a student at the University of Utah, Dr.
Robert Jarvik combined several modifications: an ovoid shape to fit inside the
human chest, a more blood-compatible polyurethane developed by biomedical
engineer Dr. Donald Lyman, and a fabrication method by Kwan-Gett that made the
inside of the ventricles smooth and seamless to reduce dangerous stroke-causing
blood clots. On December 2, 1982, Dr. William DeVries implanted the artificial
heart into retired dentist Dr. Barney Bailey Clark (born January 21, 1921), who
survived 112 days with the device, dying on March 23, 1983. Bill Schroeder
became the second recipient and lived for a record 620 days.
Contrary to popular belief and erroneous articles in several
periodicals, the Jarvik heart was not banned for permanent use. Today, the
modern version of the Jarvik 7 is known as the SynCardia temporary CardioWest Total
Artificial Heart. It has been implanted in more than 800 people as a bridge to
transplantation.
In the mid-1980s, artificial hearts were powered by dishwasher-sized
pneumatic power sources whose lineage went back to Alpha-Laval milking
machines. Moreover, two sizable catheters had to cross the body wall to carry
the pneumatic pulses to the implanted heart, greatly increasing the risk of
infection. To speed development of a new generation of technologies, the
National Heart, Lung, and Blood Institute opened a competition for implantable
electrically powered artificial hearts. Three groups received funding:
Cleveland Clinic in Cleveland, Ohio; the College of Medicine of Pennsylvania
State University (Penn State Hershey Medical Center) in Hershey, Pennsylvania;
and AbioMed, Inc. of Danvers, Massachusetts. Despite considerable progress, the
Cleveland program was discontinued after the first five years.
Polymeric trileaflet valves ensure unidirectional blood flow with a
low pressure gradient and good longevity. State-of-the-art transcutaneous
energy transfer eliminates the need for electric wires crossing the chest wall.
The first AbioCor to be surgically implanted in a patient was on July
3, 2001. The AbioCor is made of titanium and plastic with a weight of two
pounds, and its internal battery can be recharged with a transduction device
that sends power through the skin. The internal battery lasts for a half hour,
and a wearable external battery pack lasts for four hours. The FDA announced on
September 5, 2006, that the AbioCor could be implanted for humanitarian uses
after the device had been tested on 15 patients. It is intended for critically
ill patients who can not receive a heart transplant. Some limitations of the
current AbioCor are that its size makes it suitable for only about 50% of the
male population, and its useful life is only 1–2 years. By combining its valved
ventricles with the control technology and roller screw developed at Penn
State, AbioMed has designed a smaller, more stable heart, the AbioCor II. This
pump, which should be implantable in most men and 50% of women with a life span
of up to five years, had animal trials in 2005, and the company hoped to get
FDA approval for human use in 2008.
First clinical application of an intrathoracic pump
On July 19, 1963, E. Stanley Crawford and Domingo Liotta implanted the
first clinical Left Ventricular Assist Device (LVAD) at The Methodist Hospital
in Houston, Texas, in a patient who had a cardiac arrest after surgery. The
patient survived for four days under mechanical support but did not recover
from the complications of the cardiac arrest; finally, the pump was
discontinued, and the patient died.
First clinical application of a paracorporeal pump
On April 21, 1966, Michael DeBakey and Liotta implanted the first clinical
LVAD in a paracorporeal position (where the external pump rests at the side of
the patient) at The Methodist Hospital in Houston, in a patient experiencing
cardiogenic shock after heart surgery. The patient developed neurological and
pulmonary complications and died after few days of LVAD mechanical support. In
October 1966, DeBakey and Liotta implanted the paracorporeal Liotta-DeBakey
LVAD in a new patient who recovered well and was discharged from the hospital
after 10 days of mechanical support, thus constituting the first successful use
of an LVAD for postcardiotomy shock.
Recent developments
In August 2006, an artificial heart was implanted into a 15-year-old girl
at the Stollery Children's Hospital in Edmonton, Alberta. It was intended to
act as a temporary fixture until a donor heart could be found. Instead, the
artificial heart (called a Berlin Heart) allowed for natural processes to occur
and her heart healed on its own. After 146 days, the Berlin Heart was removed,
and the girl's heart was able to function properly on its own.
On December 16, 2011 the Berlin Heart, a ventricular assist intended
for children age 16 and under, gained U.S. FDA approval. The device has since
been successfully implanted in several children including a 4-year-old Honduran
girl at Children's Hospital Boston.
Total artificial heart
In June 1996, a 46-year-old Chinese American Mr. Yao ST received the Asia's
first total artificial heart implantation done by Dr. Jeng Wei at Cheng-Hsin
General Hospital in Taiwan. This pneumatic Phoenix-7 Total Artificial Heart was
manufactured by a dentist Kelvin K Cheng, a physican T.M. Kao and colleagues at
the Taiwan TAH Research Center in Tainan. With this experimental artificial
heart, the patient's BP was maintained at 90-100/40-55 mmHg and cardiac output
at 4.2-5.8 L/min. After 15 days of bridging, Mr. Yao received combined heart
and kidney transplantation. As of March 2013, he is still very well and is
currently living in San Francisco, USA. Mr. Yao ST is the world first
successful combined heart and kidney transplantation patient after bridging
with total artificial heart.
On October 27, 2008, French professor and leading heart transplant
specialist Alain F. Carpentier announced that a fully implantable artificial
heart will be ready for clinical trial by 2011 and for alternative transplant
in 2013. It was developed and will be manufactured by him, biomedical firm
CARMAT SA, and venture capital firm Truffle Capital. The prototype uses
embedded electronic sensors and is made from chemically treated animal tissues,
called "biomaterials", or a "pseudo-skin" of biosynthetic,
microporous materials. According to an interview of the professor Alain
Carpentier in Paris(2011), a number of leading cardiac
clinics already conducted successful partial replacement of the organic
components of the artificial heart, for example, replacing valves, large
vessels, atria, ventricles. In addition to cardio-surgery, there is the
medico-psychological aspect of an artificial heart. A quarter of patients in
the postoperative period after prosthetic valvular surgery,
developed a specific psychopathological symptoms, which later received the name
Skumin syndrome in 1978. It is possible that a similar problem will be
discovered when conducting large-scale operations to implant an artificial
heart.
Another U.S. team with a prototype called 2005 MagScrew Total
Artificial Heart, including Japan and South Korea researchers are racing to
produce similar projects.
In August 2010, 50-year-old Angelo Tigano of Fairfield, New South
Wales, Australia, had his failing heart removed in a five-hour operation and it
was replaced with the SynCardia temporary Total Artificial Heart by surgeon Dr
Phillip Spratt, head of the heart transplant unit at St Vincent's Hospital,
Sydney.
On 12 March 2011, an experimental artificial heart was implanted in
55-year-old Craig Lewis at The Texas Heart Institute in Houston by Drs. O. H.
Frazier and William Cohn. The device is a combination of two modified HeartMate
II pumps that is currently undergoing bovine trials.
On 9 June 2011, 40 year old Matthew Green was implanted with the SynCardia
temporary Total Artificial heart in a seven hour operation at Papworth
Hospital. He was the first Briton to leave hospital supported by an artificial
Heart on 2 August 2011.
A centrifugal pump or an axial-flow pump can be used as an artificial
heart, resulting in the patient being alive without a pulse.
This link describes a centrifugal artificial heart which alternately
pumps the pulmonary circulation and the systemic circulation, causing a pulse.
Heart assist devices
Patients who have some remaining heart function but who can no longer live
normally may be candidates for ventricular assist devices (VAD), which do not
replace the human heart but complement it by taking up much of the function.
The first Left Ventricular Assist Device (LVAD) system was created by
Domingo Liotta at Baylor College of Medicine in Houston in 1962.
Another VAD, the Kantrowitz CardioVad, designed by Adrian Kantrowitz
boosts the native heart by taking up over 50% of its function.[49]
Additionally, the VAD can help patients on the wait list for a heart
transplant. In a young person, this device could delay the need for a
transplant by 10–15 years, or even allow the heart to recover, in which case
the VAD can be removed. The artificial heart is powered by a battery that needs
to be changed several times while still working.
The first heart assist device was approved by the FDA in 1994, and two
more received approval in 1998. While the original assist devices emulated the
pulsating heart, newer versions, such as the Heartmate II, developed by The
Texas Heart Institute of Houston, provide continuous flow. These pumps (which
may be centrifugal or axial flow) are smaller and potentially more durable and
last longer than the current generation of total heart replacement pumps.
Another major advantage of a VAD is that the patient keeps the natural heart,
which may still function for temporary back-up support if the mechanical pump
were to stop. This may provide enough support to keep the patient alive until a
solution to the problem is implemented.
Several continuous-flow ventricular assist devices have been approved for
use in the European Union, and, as of August 2007, were undergoing clinical
trials for FDA approval.
Suffering from end-stage heart failure, former Vice President Dick
Cheney underwent a procedure in July 2010 to have a VAD implanted. In 2012, he
received a heart transplant at age 71 after 20 months on a waiting list.
·
Reduce body weight
·
Decrease LDL (“bad”) cholesterol levels
·
Raise HDL (“good”) cholesterol levels
·
Improve congestive heart failure
·
Protect against ischemic heart disease
·
Prevent atherosclerosis
·
Combat certain cancers
·
Act as a general antibacterial
To treat an illness, it is always in one's interest to know the cause.
Heart disease, attacks, strokes, and other coronary disorders are no exception.
Contaminated, processed foods lack nutrient value to sustain us. Fresh, organic
raw produce has been used since ancient times to nourish our bodies with needed
support.
Simply put, death begets death, life begets life. What we put into
our systems, to a large extent affects what comes out of our systems. When we
eat, drink or breathe correctly we get desired results. When we eat, drink or
breathe incorrectly, based on lifetimes of trial and error, numerous issues
known as "health disorders" can be exacerbated, and eventually the
"ol'ticker just finally gives out"... unless we get rid of the cause
in time. This can be any number of things.
The heart is a pump, pushing fresh blood out in all directions, and
refilling up with more fresh blood after the kidneys and liver do their job to
filter out impurities. Hopefully we replenish blood with more fresh, useable
nutrient sent out to all the body parts.
This keeps going on until the heart stops and we die. The heart is like an
engine in this way: When given proper fuels it works. When we feed a body the
proper types of foods and oils, it maintains function much better, and we cut
down the possibility of it stopping.
Numerous things stop the heart, yet one of the leading causes is too
much fat and grease in the blood stream, that the liver and kidneys are not
able to filter out. Steve Wynn of Las Vegas recently equated consumption of
cow's milk to drinking "liquid cholesterol".
Obesity is often the result of fat, crud, and grease, sometimes
called cholesterol and/or plaque lining the arteries, that
starts hardening from a lower temperature. There are other causes as well.
Right now we are discussing heart and stroke issues. Reversing these conditions
is essential to heart health.
Hot saturated fats can easily pass through stomach linings to the
blood stream. Away from the main vessels, we sometimes get "fatty
buildups" known as tumors, cysts, clots, fibroids, as well as fat. These
"pockets of crud, grease, etc." are part of a body's natural
mechanism to protect itself from toxic waste in the body that stomach, liver,
kidney, etc. cannot filter out of the blood, and it gets stuck somewhere else
until "further notice".
When these "pockets" build up beyond what the body can do
anything with, they can burst, leak, leading to a severe toxic reaction when
this "less than desirable crud, not crude" starts spreading out. This
is what they often call cancer, and if it spreads too fast, or the "stored
waste" does too much damage it can lead to heart failure.
Many strokes happen in in the winter, especially around Winter
Solstice when many people eat a lot of fat-rich and greasy foods for the
holidays. It is also colder, so the body generally has to work harder to
"warm up" the fat / grease in clogged arteries and veins.
This is why exercising is good, as it warms up this fat / grease, and
hopefully gets channeled out through the liver or kidneys, later through
intestinal system as excrement. Grease or cholesterol in our blood vessels
works like grease and crud in kitchen drains, clogging up systems. At least
that's how many medical professionals approach the body - like a plumber cleans
drains or mechanic fixes a car. Poisonous drugs, chemicals, catheters,
chelation, and invasive treatments are sometimes prescribed to flush out this
harmful plaque, cholesterol, and/or grease build-up that restricts blood flow.
A classic example: When John Robbins wrote and later filmed Diet for
a New America he worked with Dr. Michael Klaper, M.D. / founder at the
Institute of Nutrition Education and Research. They did a "before and
after" test with a gentleman eating a standard beef cheese burger. Before
the test blood was extracted in a test tube, and was red. 1/2 hour AFTER eating
the cheese burger, his blood was once again extracted and at the top of the red
blood in the test tube was app. 1/2" of "white puss". This is
because fat from the burger heads right through the lining of the stomach,
hitting the blood stream, proving fat from animal products is a leading cause
of the hardening and clogging of arteries.
A heart attack can be from numerous causes, yet many are all related,
as our bodies are designed so all parts synchronize for maximum efficiency. One
part not working properly often affects all other parts of the body. This is
the Holistic approach, looking at all body functions to realize why there is a
problem if one exists.
Anger and/or emotional stress often have huge impact on our hearts. Being caught in extremely polluted places, especially while eating
junk foods, smoking, taking dangerous drugs, etc. can exacerbate the symptom of
heart stress, even causing lung / heart ache at times. Even intense
performance or exercise can greatly affect heart rates, so be careful. Take
these symptoms serious, if they do not dissipate after a number of minutes.
Heart disease is rampant with a population that eat,
drink or breathe contaminated toxins that exist in a wide variety of
environments, diets, and lifestyles. It takes a lot of stamina, discipline and
change to sometimes accomplish a truly healthy relationship between body, mind
and Spirit. A good start is to avoid the deleterious effects of drugs,
chemicals, and poisons that are prevalent in today's society.
These symptoms, caused by fat coagulating throughout the blood stream
of arteries and veins, can lead to many illnesses, and is a major contributor
to heart disease and strokes. This adverse condition can be reversed, yet takes
time and patience.
The best case is prevention, and there is not a better time than now
to start. Most larger communities now have natural
foods groceries, and that is a good place to make a shift, as well as your own
organic gardens. Realize that what you put into yourself is what leads to
numerous body reactions. Vegan [pure vegetarian - no animal
products], fresh raw organic produce, nuts, seeds, fresh fruits, pure juices,
while avoiding wheat is a good start. Nutritional balance is essential
in maintaining good health.
Veins and arteries in our bodies accumulate junk just like homes and
yards, if they are not cleaned up. When passage ways to the heart are totally
blocked, that's it. Sometimes heart attacks, leading to an emergency hospital
visit will only exacerbate the problem, or at best prolong it while one is
dying in pain. Open heart surgery has saved lives, yet it is very expensive,
leading to an extended life of more pain and suffering in most cases. Although
frustrating, sometimes death is the only other option at this point.
The best plan - eat healthy foods while avoiding greasy food,
especially contaminated animal products, those with a lot of fat. Cream,
cheese, butter, lard, and hydrogenated oils [Crisco included] are out.
One of my favorites is carrot / beet / celery juice. This juice is
best when freshly made, drinking it within 15 minutes of juicing it, as all
these great enzymes and body maintenance nutrients are most active when fresh.
Once this formula enters our systems, it is immediately absorbed by stomach and
digestive tract, entering blood stream and affecting all parts of our cellular
structure to some extent.
Beets have been known to effectively reduce blood pressure without the
dangerous drug prescriptions designed to do this.
Carrots are great for helping maintain and rebuild skin / body tissue.
Celery helps balance carrots and beets. Celery contains pthalides, which
have been shown to lower blood pressure by relaxing the muscles around the
arteries and allowing vessels to dilate. The calcium, magnesium, and potassium
in celery also helps regulate blood pressure.
Fruits and vegetables whose edible sections are white may lower your
risk of stroke more than other fruits and vegetables, Dutch researchers report.
How To Improve Cholesterol Levels
Realize the HDL cholesterol is essential to health, the kind a body
naturally makes to maintain itself. LDL cholesterol is not good, a condition
existing from consumption of saturated fats of animal products that has entered
the blood stream, lodging itself there. Here are ways to reduce this extreme
problem with many people:
Eat more nuts. Australian scientists witnessed men replacing 15 percent of
daily calorie intake with macadamia nuts [12 to 16 nuts per day] and their HDL
levels went up by 8 percent. You can even eat nuts covered in chocolate or
rolled in cocoa powder. Japanese find that polyphenols in chocolate activate
genes increasing HDL production. Analyzing 25 different studies on walnuts,
pecans, almonds, peanuts, pistachios, and macadamia nuts, Loma Linda University
researchers found eating 67 grams of nuts per day—that’s a little more than two
ounces—increased the ratio of HDL to LDL in the blood by 8.3 percent.
Exercising, moving all body parts while staying active is also essential to
better health. Either get out in your yard, walk or
run the dog, bicycling, etc. When you have no yard work or strenuous chores, go
to a gym. 20 minutes or more is great, as each extra minute increases HDL.
Cranberry and grapefruit juices help lower body LDL cholesterol.
Avoid extreme hunger: A British Medical Journal study found people eating
six or more small meals a day have 5 percent lower LDL cholesterol levels than
those eating one or two large meals.
Oatmeal: Consuming oatmeal is much superior to wheat products, and is
packed with nutrient. Men in a University of Connecticut study with high LDL
cholesterol (above 200 mg/dL) eating oat-bran cookies daily for 8 weeks dropped
their levels by more than 20 percent.
Concord Grapes: Researchers from University of California find compounds in
Concord grapes help slow formation of artery-clogging LDL cholesterol. Grapes
lower blood pressure by average of 6 points when drinking 12 ounces of juice
per day.
Consider the Vegan Diet: Toronto researchers find men adding a couple of
vegetarian servings, a fare such as whole grains, nuts, and beans to the diet
each day for a month, can lower LDL cholesterol by nearly 30 percent.
Dark Chocoloate: Avoid milk chocolate, and/or conventional chocolates
containing milk fat. Read the ingredients, as these kind
can form LDL cholesterol. Researchers from Finland find consuming 2.5 ounces of
dark chocolate each day boosts levels of HDL by between 11 and 14 percent.
Green Tea: According to Harvard Women's Health Watch
benefits for regular consumers of green and black teas include a reduced risk for
heart disease. The antioxidants in green, black, and oolong teas can help block
the oxidation of LDL (bad) cholesterol, increase HDL (good) cholesterol and
improve artery function.
Once you make the change away from foods making LDL cholesterol along
with other non essential saturated and trans fats,
stay away from those food groups. Continuing to eat them later will simply
bring back the problem.
A few years back one of my best friends would eat a pint of ice cream
every night, after eating greasy Chinese food every day. Out of concern, I
cautioned him about this, but he "felt" healthy as he was active,
working from dawn to dusk every day. On one day in particular, he was not
feeling good, keeled over and died. When paramedics came, they said it was such
a massive heart failure, that even if he made it to a hospital, only 2 out of
100 survive such a severe attack.
There is always hope for a better life when one changes before it is
too late. This does not mean we live forever, as a time will come when we all
pass on. Would you prefer this life to be more pleasant, with less health
issues to deal with? Then you are at the right site to learn ways you can heal
yourself, while saving your family inheritance / estate for future generations,
if the Health Care Profession doesn't take it all from letting adverse
conditions go too far. Most insurance plans often do not cover the entire
amount of treatment procedure, so prevention is often the best remedy or
solution.
When time permits, this page will continue with much more pertinent
information, to help individuals treat heart disease naturally, as well as
guidelines to prevent the debilitating and often deadly illness. For now, check
out the numerous links below to get a better understanding how heart problems
can be avoided.
VIDEO
The Heart Anatomy
http://www.youtube.com/watch?v=Y8AgVTlcvDQ
REFERENCES:
1. DuBose
TJ, Cunyus JA, and Johnson L (1990). "Embryonic Heart Rate and Age".
J Diagn Med Sonography 6 (3): 151–157. doi:10.1177/875647939000600306
2. Kumar; Abbas; Fausto (2005). Robbins and Cotran Pathologic Basis of Disease (7th ed.).
Philadelphia: Elsevier Saunders. p. 556. ISBN 0-7216-0187-1.
3. Marieb,
Elaine Nicpon (2003). Human Anatomy & Physiology (6th ed.). Upper Saddle
River: Pearson Education. ISBN 0-8053-5463-8.
4. Paul Marchand The anatomy and applied anatomy of the mediastinal
fascia. Retrieved 2013-02-27.