Download Heart Valves

Anatomy and physiology of the heart
The heart is composed of three layers :1- The inner layer, or endocardium, consists of endothelial
tissue and lines the inside of the heart and valves.
2- The middle layer, or myocardium, is made up of muscle
fibers and is responsible for the pumping action.
3-The exterior layer of the heart is called the epicardium.
-The heart is encased in a thin, fibrous sac called the
pericardium, which is composed of two layers. Adhering to
the epicardiumis the visceral pericardium. Enveloping the
visceral pericardium is the parietal pericardium, a tough
fibrous
tissue
that
attaches
to
the
great vessels, diaphragm, sternum, and vertebral column and
supports the heart in the mediastinum. The space between
these two layers (pericardial space) is filled with about 30 mL
of fluid, which lubricates the surface of the heart and reduces
friction during systole.
Heart Chambers:The four chambers of the heart constitute the right- and left
sided pumping systems. The right side of the heart, made up of
the right atrium and right ventricle, distributes venous blood
(deoxygenated blood) to the lungs via the pulmonary artery
(pulmonary circulation) for oxygenation. The right atrium
receives blood returning from the superior vena cava
(head,neck, and upper extremities), inferior vena cava (trunk
and
lower
extremities),
and
coronary
sinus
(coronary
circulation). The left side of the heart, composed of the left
atrium and left ventricle, distributes oxygenated blood to the
remainder of the body via the aorta (systemic circulation). The
left atrium receives oxygenated blood from the pulmonary
circulation via the pulmonary veins. The relationships of the
four heart chambers are shown in The varying thicknesses of the
atrial and ventricular walls relate to the workload required by
each chamber. The atria are thin-walled because blood returning
to these chambers generates low pressures. In contrast, the
ventricular
walls
are
thicker
because they generate greater pressures during systole. The right
ventricle contracts against low pulmonary vascular pressure and
has thinner walls than the left ventricle. The left ventricle, with
walls two-and-a-half times more muscular than those of the
right ventricle, contracts against high systemic pressure.
Because the heart lies in a rotated position within the chest
cavity, the right ventricle lies anteriorly (just beneath the
sternum) and the left ventricle is situated posteriorly. The left
ventricle is esponsible for the apex beat or the point of
maximum impulse (PMI), which is normally palpable in the left
midclavicular line of the chest wall at the fifth intercostal space.
Heart Valves:The four valves in the heart permit blood to flow in only one
direction. The valves, which are composed of thin leaflets of
fibrous tissue, open and close in response to the movement of
blood and pressure changes within the chambers. There are two
types of valves: atrioventricular and semilunar
ATRIOVENTRICULAR VALVES:The valves that separate the atria from the ventricles are termed
atrioventricular valves. The tricuspid valve, so named because it
is composed of three cusps or leaflets, separates the right atrium
from the right ventricle. The mitral, or bicuspid (two cusps)
valve, lies between the left atrium and the left ventricle
Normally, when the ventricles contract, ventricular pressure
rises, closing the atrioventricular valve leaflets. Two additional
structures, the papillary muscles and the chordae tendineae,
maintain valve closure. The papillary muscles, located on the
sides of the ventricular walls, are connected to the valve leaflets
by thin fibrous bands called chordae tendineae. During systole,
contraction of the papillary muscles causes the chordae
tendineae
to
become
taut,
keeping
the
valve
leaflets
approximated and closed.
SEMILUNARVALVES:The two semilunar valves are composed of three half-moon-like
leaflets. The valve between the right ventricle and the
pulmonary artery is called the pulmonic valve; the valve
between the left ventricle and the aorta is called the aortic valve
FUNCTIONOFTHEHEART:CONDUCTIONSYSTEM:The specialized heart cells of the cardiac conduction system
methodically generate and coordinate the transmission of
electrical impulses to the myocardial cells. The result is
sequential atrioventricular contraction, which provides for the
most effective flow of blood, thereby optimizing cardiac output.
Three physiologic characteristics of the cardiac conduction cells
account
Automaticity:-
for
ability
this
to
initiate
coordination:
an
electrical
impulse
Excitability:- ability to respond to an electrical impulse
Conductivity:- ability to transmit an electrical impulse from one
cell to another.
The sinoatrial (SA) node, referred to as the primary pacemaker
of the heart, is located at the junction of the superior vena
cava and the right atrium. The SA node in a normal
resting heart has an inherent firing rate of 60 to 100 impulses per
minute, but the rate can change in response to the metabolic
demands of the body. The electrical impulses initiated by the SA
node are conducted along the myocardial cells of the atria via
specialized tracts called inter nodal pathways. The impulses
cause electrical stimulation and subsequent contraction of the
atria.
The
impulses
are
then
conducted to the atrioventricular (AV) node. The AV node
(located in the right atrial wall near the tricuspid valve) consists
of another group of specialized muscle cells similar to those of
the SA node. The AV node coordinates the incoming electrical
impulses from the atria and, after a slight delay (allowing the
atria time to contract and complete ventricular filling), relays the
impulse to the ventricles. This impulse is then conducted
through a bundle of specialized conduction cells (bundle of His)
that travel in the septum separating the left and right ventricles.
The bundle of His divides into the right bundle branch
(conducting impulses to the right ventricle) and the left bundle
branch (conducting impulses to the left ventricle). To transmit
impulses to the largest chamber of the heart,
Physiology of Cardiac Conduction:Cardiac electrical activity is the result of the movement of ions
(charged particles such as sodium, potassium, and calcium)
across the cell membrane. The electrical changes recorded
within a single cell result in what is known as the cardiac action
potential In the resting state, cardiac muscle cells are polarized,
which means an electrical difference exists between the
negatively charged inside and the positively charged outside of
the cell membrane. As soon as an electrical impulse is initiated,
cell membrane permeability changes and sodium moves rapidly
into the cell, while potassium exits the cell. This ionic exchange
begins depolarization (electrical activation of the cell),
converting the internal charge of the cell to a positive one.
Contraction of the myocardium follows depolarization. The
interaction between changes in membrane voltage and muscle
contraction is called electromechanical coupling. As one cardiac
muscle cell is depolarized, it acts as a stimulus to its neighboring
cell, causing it to depolarize. Sufficient depolarization of a
single
specialized
conduction
system
cell
results
in
depolarization and contraction of the entire myocardium.
Repolarization (return of the cell to its resting state) occurs as
the cell returns to its baseline or resting state; this corresponds to
relaxation of myocardial muscle.
CARDIAC CYCLE:-
Beginning with systole, the pressure inside the ventricles rapidly
rises, forcing the atrioventricular valves to close. As a result,
blood ceases to flow from the atria into the ventricles and
regurgitation (backflow) of blood into the atria is prevented. The
rapid rise of pressure inside the right and left ventricles forces
the pulmonic and aortic valves to open, and blood is ejected into
the pulmonary artery and aorta, respectively. The exit of blood
is at first rapid then, as the pressure in each ventricle and its
corresponding artery equalizes, the flow of blood gradually
decreases. At the end of systole, pressure within the right and
left ventricles rapidly decreases. This lowers pulmonary artery
and aortic pressure, causing closure of the semilunar valves.
These events mark the onset of diastole. During diastole, when
the ventricles are relaxed and the atrioventricular valves are
open, blood returning from the veins flows into the atria and
then into the ventricles. Toward the end of this diastolic period,
the atrial muscles contract in response to an electrical impulse
initiated by the SA node (atrial systole). The resultant
contraction raises the pressure inside the atria, ejecting
blood into the ventricles.
Cardiac Output:Cardiac output is the amount of blood pumped by each
ventricle during a given period. The cardiac output in a resting
adult is about 5 L per minute but varies greatly depending on the
metabolic needs of the body. Cardiac output is computed by
multiplying the stroke volume by the heart rate. Stroke volume
is the amount of blood ejected per heartbeat. The average resting
stroke volume is about 70 mL,
CONTROL OF HEART RATE:Changes in heart rate are accomplished by reflex controls
mediated by the autonomic nervous system, including its
sympathetic
and
parasympathetic
divisions.
The
parasympathetic impulses, which travel to the heart through the
vagus nerve, can slow the cardiac rate, whereas sympathetic
impulses increase it. These effects on heart rate result from
action on the SA node, to either decrease or increase its inherent
rate. The balance between these two reflex control systems
normally determines the heart rate. The heart rate is stimulated
also by an increased level of circulating catecholamines
(secreted by the adrenal gland) and by excess thyroid hormone,
which produces a catecholamine-like effect. Heart rate is also
affected by central nervous system and baroreceptor activity.
Baroreceptors are specialized nerve cells located in the aortic
arch and in both right and left internal carotid arteries The
baroreceptors are sensitive to changes in blood pressure (BP).
During elevations in BP (hypertension), these cells increase
their rate of discharge, transmitting impulses to the medulla.
This initiates parasympathetic activity and inhibits sympathetic
response, lowering the heart rate and the BP. The opposite is
true during hypotension (low BP). Hypotension results in less
baroreceptor stimulation, which prompts a decrease in
parasympathetic inhibitory activity in the SA node, allowing for
enhanced sympathetic activity. The resultant vasoconstriction
and
increased
heart
rate
elevate
the
BP.
Cardiac Signs and Symptoms:Patients with cardiovascular disorders commonly have one or
more of the following signs and symptoms:
1• Chest pain or discomfort (angina pectoris, MI, valvular
heartdisease)
2• Shortness of breath or dyspnea (MI, left ventricular failure,
HF)
3• Edema and weight gain (right ventricular failure, HF)
4• Palpitations (dysrhythmias resulting from myocardial
ischemia, valvular heart disease, ventricular aneurysm, stress,
electrolyte imbalance)
5• Fatigue (earliest symptom associated with several
cardiovascular disorders)
6• Dizziness and syncope or loss of consciousness (postural
hypotension, dysrhythmias, vasovagal effect, cerebrovascular
disorders)
Not all chest discomfort is related to myocardial ischemia.
When a patient has chest discomfort, questions should focus on
differentiating a serious, life-threatening condition such as MI
from conditions that are less serious or that would be treated
differently.
-The following points should be remembered
when assessing patients with cardiac symptoms:
1• Women are more likely to present with atypical symptoms
of
MI
than
are
men.
2• There is little correlation between the severity of the chest
discomfort and the gravity of its cause. Elderly people and
those with diabetes may not have pain with angina or MI
because of neuropathies. Fatigue and shortness of breath
may be the predominant symptoms in these patients.
3• There is poor correlation between the location of chest
discomfort
and
its
source.
4• The patient may have more than one clinical condition
occurring
simultaneously.
5• In a patient with a history of CAD, the chest discomfort
should be assumed to be secondary to ischemia .