Blood returning from
the systemic (body) circulation enters the right atrium (via the inferior & superior vena cavas). From there, blood flows into the right ventricle,
which then pumps blood to the lungs (via the pulmonary artery). Blood returning
from the lungs enters the left atrium (via pulmonary veins), then the left
ventricle. The left ventricle then pumps blood to the rest of the body
(systemic circulation) via the aorta.
How the heart works
How blood flows through the heart
Heart walls - 3 distinct layers:
1 - endocardium - innermost layer; epithelial tissue that lines the
entire circulatory system
2 - myocardium - thickest layer; consists of cardiac muscle
3 - epicardium - thin, external membrane around the heart
Cardiac muscle tissue:
striated (see photo below; consists of sarcomeres just like skeletal muscle)
cells contain numerous mitochondria (up to 40% of cell volume)
adjacent cells join end-to-end at structures called intercalated discs
Intercalated
discs contain two types of specialized junctions:
desmosomes (which act like rivets & hold the cells tightly together)
and
gap junctions (which permit action potentials to easily spread from
one cardiac muscle cell to adjacent cells).
Cardiac muscle tissue forms 2 functional syncytia or units:
the atria being one &
the ventricles the other.
Because of the presence of gap junctions, if any cell is stimulated within
a syncytium, then the impulse will spread to all cells. In other words,
the 2 atria always function as a unit & the 2 ventricles always function
as a unit. However, there are no gap junctions between atrial & ventricular contractile cells. In addition, the atria & ventricles
are separated by the electrically nonconductive tissue that surrounds the
valves. So, as will be discussed later, a special conducting system is
needed to permit transmission of impulses from the atria to the ventricles.
Contractile cells, of course, contract when stimulated. Autorhythmic cells,
on the other hand, are self-stimulating & contract without any external
stimulation. The action potentials that occur in these two types of cells
are a bit different:
On the left is the action potential of an autorhythmic cell; on the
right, the action potential of a contractile cell.
Autorhythmic cells exhibit PACEMAKER POTENTIALS. Depolarization
is due to the inward diffusion of calcium (not sodium as in nerve cell
membranes). Depolarization begins when:
the slow calcium channels open (4),
then concludes (quickly) when the fast calcium channels open (0).
Repolarization is due to the outward diffusion of potassium (3).
Used with permission: http://mail.bris.ac.uk/~pydml/CVS/Heart/Cells/Electrics/APpmr.htm
In Contractile cells:
depolarization is very rapid & is due to the inward diffusion
of sodium (0).
repolarization begins with a slow outward diffusion of potassium,
but that is largely offset by the slow inward diffusion of calcium (1 & 2). So, repolarization begins with a plateau phase. Then, potassium diffuses
out much more rapidly as the calcium channels close (3), and the membrane
potential quickly reaches the 'resting' potential (4).
SA node = has the highest or fastest rhythm &, therefore, sets the
pace or rate of contraction for the entire heart. As a result, the SA node
is commonly referred to as the PACEMAKER.
Begins at the SA node & quickly spreads through both atria
Also travels through the heart's 'conducting system' (AV node > AV bundle
> bundle branches > Purkinje fibers) through the ventricles
For efficient pumping:
The atria should contract (& finish contracting) before the ventricles
contract. This occurs because of AV nodal delay (that is, the impulse
travels rather slowly through the AV node & this permits the atria
to complete contraction before the ventricles begin contraction).
The atria should contract as a unit, & the ventricles should contract
as a unit. This occurs because the impulse spreads so rapidly that
all myocardial cells in the atria and ventricles, respectively, contract
at about the same time. The impulse spreads rapidly through the ventricles
because of the conducting system.
Refractory period of contractile cells:
Lasts about 250 msec (almost as long as contraction period)
The long refractory period means that cardiac muscle cannot be restimulated
until contraction is almost over & this makes summation (& tetanus)
of cardiac muscle impossible. This is a valuable protective mechanism because
pumping requires alternate periods of contraction & relaxation; prolonged
tetanus would prove fatal.
Electrocardiogram
(ECG) = record of spread of electrical activity through the heart
P wave = caused by atrial depolarization
QRS complex = caused by ventricular depolarization
T wave = caused by ventricular repolarization
ECG = useful in diagnosing abnormal heart rates, arrhythmias, & damage of heart muscle
Electrocardiogram
Coronary artery disease (CAD) is a condition in which plaque builds up inside the coronary arteries that supply heart muscle with oxygen-rich blood. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. When plaque builds up in the arteries, the condition is called atherosclerosis. Plaque narrows the arteries and reduces blood flow
to your heart muscle. It also makes it more likely that blood clots will form and partially or completely block blood flow.
When coronary arteries are narrowed or blocked, oxygen-rich blood can't reach the heart muscle. This can cause angina or a heart attack. Angina is chest pain or discomfort that occurs when not enough blood flows to an area of heart muscle. A heart attack occurs when blood flow to an area of heart muscle is completely blocked. This prevents oxygen-rich blood from reaching that area of heart muscle and causes it to die. Without quick treatment, a heart attack can lead to serious problems and even death. Over time, CAD can weaken heart muscle and lead to heart failure and arrhythmias. Heart failure is a condition in which your heart can't pump enough blood throughout your body. Arrhythmias are problems with the speed or rhythm of your heartbeat. CAD is the most common type of heart disease. It's the leading cause of death in the United States for both men and women. Lifestyle changes, medicines, and/or medical procedures can effectively prevent or treat CAD in most people (Source: NHLBI).
Heart Valves:
Atrioventricular (AV) valves - prevent backflow of blood from ventricles
to atria during ventricular systole (contraction)
Tricuspid valve - located between right atrium & right ventricle
Mitral valve - located between left atrium & left ventricle
Semilunar valves - prevent backflow of blood from arteries (pulmonary
artery & the aorta) to ventricles during ventricular diastole (relaxation)
Aortic valve - located between left ventricle & the aorta
Pulmonary valve - located between right ventricle & the pulmonary artery
(trunk)
All valves consist of connective tissue (not cardiac muscle tissue) and,
therefore, open & close passively. Valves open & close in response
to changes in pressure:
AV valves - open when pressure in the atria is greater than pressure in
the ventricles (i.e., during ventricular diastole) & closed when pressure
in the ventricles is greater than pressure in the atria (i.e., during ventricular
systole)
Semilunar valves - open when pressure in the ventricles is greater than
pressure in the arteries (i.e., during ventricular systole) and closed
when pressure in the pulmonary trunk & aorta is greater than pressure
in the ventricles (i.e., during ventricular diastole)
Heart valves & function
Cross-section of a healthy heart, including the four heart valves. The blue arrow shows the direction in which oxygen-poor blood flows from the body to the lungs. The red arrow shows the direction in which oxygen-rich blood flows from the lungs to the rest of the body.
Heart valve disease is a condition in which one or more heart valves don't work properly, making the heart
work harder and affecting its ability to pump blood.
Malfunctioning heart valves can create two basic problems: (1) Regurgitation, or backflow, occurs when a valve doesn’t close tightly. Blood leaks back into the chamber rather than flowing forward through the heart or into an artery. Backflow is most often due to prolapse (the flaps of the valve flop or bulge back into an upper heart chamber during a heartbeat). (2) Stenosis occurs when the flaps of a valve thicken, stiffen, or fuse together. This prevents the heart valve from fully opening, and not enough blood flows through the valve. You can be born with heart valve disease (congenital) or you can acquire it later in life. Although a valve may be normal at first, disease can cause problems to develop over time. Many people have heart valve defects or disease, but don't have symptoms. For some people, the condition will stay largely the same over their lifetime and not cause any problems.
For other people, the condition can worsen slowly over time until symptoms develop. If not treated, advanced heart valve disease can cause heart failure, stroke, blood clots, or sudden death due to cardiac arrest. Lifestyle changes and medicines can relieve many of the symptoms and problems linked to heart valve disease, and can also lower the risk of developing a life-threatening condition, such as stroke or sudden cardiac arrest. Eventually, however, faulty heart valves may have to be repaired or replaced (Source: NHLBI).
the first heart sound (lub) (labeled S1 below) - this
sound is generated by the closing of the AV valves (& this occurs because
increasing pressure in the ventricles causes the AV valves to close)
initially there is no change in ventricular volume (called the period
of isometric contraction) because ventricular pressure must build to a
certain level before the semilunar valves can be forced open & blood
ejected. Once that pressure is achieved, & the semilunar valves
do open, ventricular volume drops rapidly as blood
is ejected.
Ventricular diastole:
the second heart sound (dub) (labeled S2 below) -
this sound is generated by the closing of the semilunar valves (& this
occurs because pressure in the pulmonary trunk & aorta is now greater
than in the ventricles & blood in those vessels moves back toward the
area of lower pressure which closes the valves)
ventricular volume increases rapidly (period of rapid inflow) -
this occurs because blood that accumulated in the atria during ventricular
systole (when the AV valves were closed) now forces open the AV valves
(because the pressure in the atria is now greater than the pressure in
the ventricles). & flows quickly into the ventricles. After this
'rapid inflow', ventricular volume continues to increase, but at a slower
rate (the period of diastasis). This increase in volume occurs as blood
returning to the heart via the veins largely flows through the atria & into the ventricles.
equals heart rate (beats per minute) times stroke volume (milliliters of
blood pumped per beat)
typically about 5,500 milliliters (or 5.5 liters) per minute (which is
about equal to total blood volume; so, each ventricle pumps the equivalent
of total blood volume each minute under resting conditions) BUT maximum
may be as high as 25 - 35 liters per minute
Cardiac reserve:
the difference between cardiac output at rest & the maximum volume
of blood the heart is capable of pumping per minute
permits cardiac output to increase dramatically during periods of physical
activity
Effect of parasympathetic stimulation on the heart:
Increased parasympathetic stimulation > release of acetylcholine at
the SA node > increased permeability of SA node cell membranes to potassium
> 'hyperpolarized' membrane > fewer action potentials (and, therefore,
fewer contractions) per minute
a = sympathetic stimulation, b = normal heart rate, & c = parasympathetic stimulation
Effect of sympathetic stimulation on the heart:
Increased sympathetic stimulation > release of norepinephrine at SA
node > decreased permeability of SA node cell membranes to potassium >
membrane potential becomes less negative (closer to threshold) > more action
potentials (and more contractions) per minute
Regulation of Stroke Volume:
intrinsic control ==> related to amount of venous return (amount of blood
returning to the heart through the veins)
extrinsic control ==> related to amount of sympathetic stimulation
This increase in strength of contraction due to an increase in end-diastolic
volume (the volume of blood in the heart just before the ventricles begin
to contract) is called the Frank-Starling law of the heart:
Increased end-diastolic volume = increased stretching of of cardiac muscle
= increased strength of contraction = increased stroke volume
Increased sympathetic stimulation > increased strength of contraction of
cardiac muscle
Mechanism = sympathetic stimulation > release of norepinephrine > increased
permeability of muscle cell membranes to calcium > calcium diffuses in
> more cross-bridges are activated > stronger contraction
Flow rate through blood vessels
directly proportional to the pressure gradient
inversely proportional to vascular resistance
Flow = Difference in pressure/resistance
Pressure Gradient = difference in pressure between beginning & end
of vessel (pressure = force exerted by blood against vessel wall & measured in millimeters of mercury)
Resistance:
hindrance to blood flow through a vessel caused by friction between blood & vessel walls
is inversely proportional to radius to the fourth power (so, for example,
doubling the radius of a vessel decreases the resistance 16 times which,
in turn, increases flow through the vessel 16 times)
serve as passageways for blood from heart to tissues
act as pressure reservoirs because the elastic walls collapse inward during
ventricular diastole (when there is less blood in the arteries):
blood pressure averages 120 mm Hg during systole (systolic pressure) &
80 mm Hg during diastole (diastolic pressure) (& the difference between
systolic & diastolic pressures is called the pulse pressure)
Arterioles:
distribute cardiac output among systemic organs (whose needs vary over
time)
Resistance (&, therefore, blood flow) varies as a result of VASODILATION
& VASOCONSTRICTION
Factors that influence radius of arterioles:
intrinsic (or local) control
extrinsic control
Intrinsic (local) control:
changes within a tissue that alter the radius of blood vessels & adjust blood flow
especially important in skeletal muscles, the heart, & the brain
increased blood flow in an active tissue results from active hyperemia:
Increased tissue (metabolic) activity > increases levels of carbon dioxide
& acid in the tissue & decreases levels of oxygen > these changes
in the concentrations of acid, CO2, & O2 cause
smooth muscle in the walls of the arterioles to relax & this, in turn, causes vasodilation of the arterioles > vasodilation reduces resistance
with the vessel &, as a result, blood flow through the vessel increases
So, blood flow increases when a tissue (e.g., skeletal muscle) becomes
more active & the increased blood flow delivers the needed oxygen & nutrients.
Extrinsic control occurs via:
sympathetic division of the Autonomic Nervous System
parasympathetic division of the Autonomic Nervous System
The sympathetic division innervates blood vessels throughout the body while
the parasympathetic division innervates blood vessels of the external genitals.
Varying degrees of stimulation of these two divisions, therefore, can influence
arterioles (& blood flow) throughout the body.
Capillaries
Capillaries:
site of exchange of materials between blood & tissues
exchange may occur by simple diffusion
diffusion enhanced by:
thin capillary walls (just one cell thick)
narrow capillaries (so the red blood cells & plasma are close to the
walls)
large numbers (the human body has 10 - 40 billion capillaries!) which translates
into a tremendous amount of surface area through which exchange can occur
relatively slow flow of blood (providing more time for exchange to occur)
exchange also occurs through pores (located between the cells the form
the capillary walls), by vesicular transport (e.g., pinocytosis), & by bulk flow
protein-free plasma filters out of capillaries, mixes with surrounding
interstitial fluid, & is then reabsorbed. Plasma filters out at the
arteriole end of capillaries because hydrostatic (blood) pressure (an outward
force) exceeds osmotic pressure (an inward force). At the venous end of
capillaries, the filtrate tends to move back in because osmotic pressure
now exceeds hydrostatic pressure (check this animation at mcgraw-hill.com).
because the outward force at the arteriole end exceeds the inward force
at the venous end, more plasma filters out than moves back in to the capillaries.
So, fluid tends to accumulate in the tissues. The lymph vessels pick up
this fluid & transport it back to the blood.
BULK FLOW:
1 - not very important in exchange (much more exchange occurs by way
of diffusion)
2 - important in regulating the 'distribution' of fluids between the
plasma & interstitial fluid (which is important in maintaining normal
blood pressure)
serve as low-resistance passageways to return blood from the tissues to
the heart
serve as a BLOOD RESERVOIR (under resting conditions nearly two-thirds
of all your blood in located in the veins) &, therefore, the veins
are important in permitting changes in stroke volume
Cross-section of a healthy heart, including the four heart valves. The blue arrow shows the direction in which oxygen-poor blood flows from the body to the lungs. The red arrow shows the direction in which oxygen-rich blood flows from the lungs to the rest of the body.
turn, causes vasodilation of the arterioles > vasodilation reduces resistance
with the vessel &, as a result, blood flow through the vessel increases
