The Cardiovascular System

BIO 301
Human Physiology
Cardiovascular system

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The Cardiovascular System:
consists of the heart plus all the blood vessels
transports blood to all parts of the body in two 'circulations': pulmonary (lungs) & systemic (the rest of the body)
Heart:
hollow, muscular organ
4 chambers: 2 atria (right & left) & 2 ventricles (right & left)
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.

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.
In cardiac muscle, there are two types of cells:
contractile cells &
autorhythmic (or automatic) cells.
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).

Most of the muscle cells in the heart are contractile cells. The autorhythmic cells are located in these areas:
Sinoatrial (SA), or sinus, node
Atrioventricular (AV) node
Atrioventricular (AV) bundle (also sometimes called the bundle of His)
Right & left bundle branches
Purkinje fibers
Various automatic cells have different 'rhythms':
SA node - 60 - 100 per minute (usually 70 - 80 per minute)
AV node & AV bundle - 40 - 60 per minute
Bundle branches & Purkinje fibers - 20 - 40 per minute
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.

Spread of cardiac excitation:
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.

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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.

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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

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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)

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Mechanical Events of the Cardiac Cycle: (also check www-medlib.med.utah.edu/kw/pharm/hyper_heart1.html)
the cardiac cycle has two phases: systole (contraction) & diastole (relaxation)
'Electrical' events are correlated with the 'mechanical' events:
P wave = atrial depolarization = atrial systole
QRS complex = ventricular depolarization = ventricular systole (& atrial diastole occurs at the same time)
T wave = ventricular repolarization = ventricular diastole
What happens in the heart during each 'mechanical' event:
Atrial systole (labeled AC below):
no heart sounds (because no heart valves are opening or closing)
a slight increase in ventricular volume because blood from the atria is pumped into the ventricles
Ventricular systole:
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.

Used with permission: http://mail.bris.ac.uk/~pydml/CVS/Heart/Whole/CardCyc/CCprvo.htm




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Cardiac output:
volume of blood pumped by each ventricle
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
What factors permit variation in cardiac output?
Changes in heart rate:
Parasympathetic stimulation - reduces heart rate
Sympathetic stimulation - increases heart rate
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

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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
Intrinsic control:
Increased end-diastolic volume = increased strength of cardiac contraction = increased stroke volume
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

Source: http://www.sci.sdsu.edu/Faculty/Paul.Paolini/ppp/lecture21/sld006.htm
Extrinsic control:
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

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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
major determinant = vessel diameter (or radius)
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)


Source: http://www.oucom.ohiou.edu/CVPhysiology/H003.htm

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Arteries:
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)
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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.

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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
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.
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)

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Veins:
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