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VET 223 2/28-3/7
PHYSIOLOGY OF CARDIAC MUSCLE
The atrial and ventricular types of muscle contract in much the same way as skeletal muscle, except that the duration of contraction is much longer.
Heart action potential conduction system
The heart’s AP conduction system consists of weakly contractile cardiac muscle cells called autorhythmic cells that are specialized for generation and distribution of AP throughout the myocardium. These cells are located in the Sinoatrial (SA) node, Atrioventricular node (AV) node and through the Purkinje fibers.
Mechanism of the AP conduction system
The resting membrane potential of the SA fiber between discharges is about –55 to –60 millivolts, in comparison with –85 to –90 millivolts for the ventricular muscle fiber.
The cause of this lower negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium ions (via Na+ “funny current” channels), therefore positive charges entering (sodium ions) progressively neutralize some of the intracellular negativity (until reaching a “threshold level of around - 40mV).
Cardiac muscle has three main types of membrane ion channels that play very important roles in causing the voltage changes of the action potential:
Sodium voltage gated Na+ channels; same as in neurons – mainly inactive in the AP conduction system because
The resting potential in the SA node is much less negative—only –55 millivolts in the nodal fiber instead of the –70 millivolts in neurons.
At this level of –55 millivolts, the fast sodium channels mainly have already become inactivated or blocked.
This is because any time the membrane potential remains less negative than about –55 millivolts for more than a few milliseconds, the inactivation gates on the inside of the cell membrane become closed and remain so (remember from neuronal AP generation?).
Therefore, only the voltage gated calcium channels (se bellow) can open (i.e., can become activated) and thereby cause the action potential.
As a result, the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle (SA node about 80 – 120 depolarizations per minute – normal heart rate!!).
Voltage gated calcium channels (fast - new! For AP generation)
Potassium channels (same as in neurons – work in repolarization)
Steps in creation and conduction of heart action potentials
Heart AP conduction starts at the sinoatrial (SA) node (cardiac pacemaker), located between top of right atrium and cranial vena cava.
SA node contains autorhythmic cells called pacemaker cells that spontaneously initiate action potentials at a rate of ≈100 times/min.
The pacemaker cells in the SA node are muscle cells, so the SA node is a myogenic pacemaker that does not require excitation by nervous system to create slow response APs.
SA node APs are initiated in pacemaker cells using If channels in their plasma membranes.
If stands for “funny current”
If channels leak Na+ into the pacemaker cells until the membrane potential (Vm) reaches about -50 to – 40 mV, this triggers the opening of voltage-gated Ca+2 channels
Ca+2 will flow through these channels bringing + charge to inside of cell eventually reaching ~ +10 mV -> depolarization!
Repolarization of the pacemaker cells involves closing of the voltage-gated Ca+2 channels and opening of voltage-gated K+ channels (same as in the neuron!).
K+ flows out of the cell and brings the cells back to -55 to -60 mV.
After the membrane repolarizes back to-60 mV (VRest), the If channels open and leak Na+, thus starting the process of depolarization for the next heartbeat.
From the pacemaker cells of the SA node, AP spreads through gap junctions over both atria, which then contract (atrial systole).
Atria and ventricles are separated by a sheet of nonconductive connective tissue so atrial AP does NOT spread directly to ventricular myofibers through gap junctions.
To excite ventricular muscle cells, AP from SA node travels through the internodal pathway to the atrioventricular (AV) node, which is the only electrical connection between atria and ventricles.
The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions.
This slowing down allows both atria to complete their contractions before the ventricles begin to contract.
The AV node also has endogenous pacemaker activity (depolarizes ≈40 to 60 times/min), but it is slower than SA node (≈100/min).
From the AV node, APs move to the atrioventricular bundle.
AP spreads from AV bundle into the right and left bundle branches, which run through the interventricular septum, to the apex of the heart and up both sides of the heart.
Purkinje fibers branch off of the bundle branches and conduct fast response AP into the contractile muscle cells of the ventricular myocardium and papillary muscles.
Special Purkinje fibers lead from the A-V node through the A-V bundle into the ventricles.
The rapid transmission of APs by Purkinje fibers is believed to be caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells.
Note: This heart action potential conduction system leads to a coordinated contraction of the ventricular myocardium (ventricular systole) from the apex (bottom, cone end of the heart) up to the base (atrio-ventricular connection), which facilitates the squeezing out of the blood from the ventricles into the large arteries.
Cardiac muscle anatomy
The intercalated discs are cell membranes that separate individual cardiac muscle cells from one another.
Cardiac muscle fibers are made up of many individual cells connected in series and in parallel with one another.
At each intercalated disc, the cell membranes fuse with one another to form permeable communicating junctions (gap junctions) that allow rapid diffusion of ions.
Therefore, from a functional point of view, ions move with ease in the intracellular fluid along the longitudinal axes of the cardiac muscle fibers so that action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.
Thus, cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one cell becomes excited, the action potential rapidly spreads to all of them.
The heart actually is composed of two syncytia.
The atrial syncytium, which constitutes the walls of the two atria; and
The ventricular syncytium, which constitutes the walls of the two ventricles.
The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular openings between the atria and ventricles.
Normally, potentials are not conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue.
Instead, they are only conducted by way of a specialized conductive system called the A-V bundle, a bundle of conductive fibers several millimeters in diameter (you already know this!).
This division of the muscle of the heart into two functional syncytia allows the atria to contract a short time ahead of ventricular contraction, which is important for the effectiveness of heart pumping.
Action potentials in cardiac muscle
During the action potential generation of a cardiac muscle fiber the intracellular potential rises from a very negative value between beats, about −85 millivolts, to a slightly positive value, about +20 millivolts, during each beat.
After the initial spike, the membrane remains depolarized for about 0.2 second, exhibiting a plateau, followed at the end of the plateau by abrupt repolarization.
The presence of this plateau in the action potential causes ventricular contraction to last as much as 15 times longer in cardiac muscle than in skeletal muscle.
What Causes the Long Action Potential and Plateau in Cardiac Muscle?
In cardiac muscle, the action potential is caused by opening of two types of channels:
Similar voltage activated fast sodium channels as those in neurons and skeletal muscle; and
Voltage gated calcium channels (slower)
This second group of channels differs from the fast sodium channels in that they are slower to open and, even more importantly, remain open for several tenths of a second.
During cardiac muscle depolarization, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this activity maintains a prolonged period of depolarization, causing the plateau in the action potential.
Furthermore, the calcium ions that enter during this plateau phase activate the muscle contractile process, this is different from the calcium ions that cause skeletal muscle contraction that are derived from the intracellular sarcoplasmic reticulum.
Another major functional difference between cardiac muscle and skeletal muscle is that the when the slow voltage calcium gated channels are open, the permeability of the cardiac muscle membrane for potassium ions decreases about fivefold, an effect that does not occur in skeletal muscle.
The decreased potassium permeability greatly decreases the efflux of positively charged potassium ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level.
When the slow calcium channels do close at the end of 0.2 to 0.3 second, and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly.
This rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
Phases of Cardiac Muscle Action Potential
Phase 0 (Depolarization):
Fast Sodium Channels Open.
When the cardiac cell is stimulated and depolarizes, the membrane potential becomes more positive.
Voltage-gated sodium channels (fast sodium channels) open and permit sodium to rapidly flow into the cell and depolarize it.
The membrane potential reaches about +20 millivolts before the sodium channels close.
Phase 1 (Initial Repolarization):
Fast Sodium Channels Close.
The sodium channels close, the cell begins to repolarize, and potassium ions leave the cell through open voltage gated potassium channels (similar to what we see in the neuron).
Phase 2 (Plateau):
“Slower” voltage gated calcium Channels Open.
A brief initial repolarization occurs (because of the fast opening of the voltage gated potassium channels), however the action potential then plateaus as a result of increased calcium ion permeability through the “slower” voltage gated calcium channels.
The voltage-gated calcium ion channels open slowly during phases 1 and 0, and calcium enters the cell.
The continuous escape of potassium ions outside of the cell and of calcium ions inside of the cell causes the cardiac muscle plateau in the action potential.
During this phase it is also thought that the permeability for potassium ions is reduced with some researchers describing two different potassium channels (fast and slow) that work during this phase. For this course, we will focus on the interrelationship of the “slower” calcium channels and the voltage gated potassium channels.
Phase 3 (Rapid Repolarization):
“Slower” Calcium Channels Close
The closure of calcium ion channels and increased potassium ion permeability (through the voltage gated potassium channels), permits potassium ions to exit the cell rapidly, ends the plateau and returns the cell membrane potential to its resting level.
Phase 4 (Resting Membrane Potential):
This averages about−80 to −90 millivolts.
Refractory Period of Cardiac Muscle
Cardiac muscle, like all excitable tissue, is refractory to restimulation during the action potential. Therefore, the refractory period of the heart is the interval of time during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle.
The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about the duration of the prolonged plateau action potential.
There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult to excite than normal but can be excited by a very strong excitatory signal, as demonstrated by the early premature contraction.
The refractory period of atrial muscle is much shorter than that for the ventricles (about 0.15 second for the atria compared with 0.25 to 0.30 second for the ventricles).
Excitation-contraction coupling— function of calcium ions and the transverse tubules
As is true for skeletal muscle, when an action potential passes over the cardiac muscle membrane, the action potential spreads to the interior of the cardiac muscle fiber along the membranes of the transverse (T) tubules.
The T tubule action potentials then act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum.
In another few thousandths of a second, these calcium ions diffuse into the myofibrils and catalyze the chemical reactions that promote sliding of the actin and myosin filaments along one another, which produces the muscle contraction.
This mechanism of excitation-contraction coupling is the same as that for skeletal muscle, but there is a second effect that is quite different.
In addition to the calcium ions that are released into the sarcoplasm from the sarcoplasmic reticulum, calcium ions also diffuse into the sarcoplasm from the T tubules at the time of the action potential (Ca++ entering from the extra cellular fluid).
Calcium entering the cell then activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum membrane, triggering the release of more calcium into the sarcoplasm (calcium dependent calcium release).
Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction by the same basic mechanism as that described for skeletal muscle.
Without the calcium the extracellular fluid, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction.
The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids. In fact, a heart placed in a calcium free solution will quickly stop beating.
Note: The T tubules of cardiac muscle are much more developed than in skeletal muscle, so in reality extracellular calcium readily enters the T tubules and binds to mucopolysaccharides located inside the T Tubules “waiting” for an AP to reach the T tubules, thus activating special Ca++ voltage gated channels that will then release the Ca++ ions into the sarcoplasm. However, since the Ca++ concentration inside the T tubules is highly dependent of the concentration of Ca++ in the extracellular fluid in this course, we will just consider extracellular calcium as triggering the release of sarcoplasmic reticulum calcium and itself entering the cell to cause cardiac muscle contraction.
* Now that we have learned how the AP starts in the cardiac conduction system (SA node) and how it spreads through the cardiac muscle to then cause muscle contraction we need to review the AP conduction pathway and understand its importance.
Conduction of heart action potentials (Summary)
The impulse (AP) is generated in the SA node.
The impulse spreads at moderate velocity through the atria but is delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal A-V bundle.
Once it has entered this bundle, it spreads very rapidly through the Purkinje fibers to the entire endocardial surfaces of the ventricles.
The impulse once again spreads slightly less rapidly through the ventricular muscle to the epicardial surfaces
Control of excitation and conduction in the heart
The impulse normally arises in the sinus node.
In some abnormal conditions, this is not the case.
Other parts of the heart can also exhibit intrinsic rhythmical excitation in the same way as the sinus nodal fibers; this is particularly true of the A-V nodal and Purkinje fibers.
The A-V nodal fibers, when not stimulated from some outside source, discharge at an intrinsic rhythmical rate of 40 to 60 times per minute, and the Purkinje fibers discharge at a rate somewhere between 15 and 40 times per minute.
These rates are in contrast to the normal rate of the sinus node of 70 to 80 times per minute.
Why does the sinus node rather than the A-V node or the Purkinje fibers control the heart’s
rhythmicity?
The answer derives from the fact that the discharge rate of the sinus node is considerably faster than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers.
Each time the sinus node discharges, its impulse is conducted into both the A-V node and Purkinje fibers, also discharging their excitable membranes.
However, the sinus node discharges again before either the A-V node or Purkinje fibers can reach their own thresholds for self-excitation.
Therefore, the new impulse from the sinus node discharges both the A-V node and Purkinje fibers before self-excitation can occur in either of these sites
Why is the order and pathway of the cardiac AP so important?
Abnormal Pacemakers—Ectopic Pacemaker
Under rarer conditions, a place in the atrial or ventricular muscle develops excessive
excitability and becomes the pacemaker.
A pacemaker elsewhere than the sinus node is called an ectopic pacemaker.
An ectopic pacemaker causes an abnormal sequence of contraction of the different parts of the heart and can cause significant weakening of heart pumping.
When A-V block occurs (when the cardiac impulse fails to pass from the atria into the ventricles through the A-V nodal and bundle system) the atria continue to beat at the normal rate of rhythm of the sinus node while a new pacemaker usually develops in the Purkinje system of the ventricles and drives the ventricular muscle at a new rate, somewhere between 15 and 40 beats per minute.
During these 5 to 20 seconds, the ventricles fail to pump blood, and the individual faints after the first 4 to 5 seconds because of lack of blood flow to the brain.
This delayed pickup of the heartbeat is called Stokes - Adams syndrome.
If the delay period is too long, it can lead to death.
The control of the Autonomic Nervous System over cardiac contraction
Sympathetic and parasympathetic nerves control heart rhythmicity and impulse conduction by the cardiac nerves
The parasympathetic nerves (the vagus nerve) are distributed mainly to the SA and AV nodes, to a lesser extent to the muscle of the two atria, and very little directly to the ventricular muscle.
The sympathetic nerves, conversely, are distributed to all parts of the heart, with strong representation in the ventricular muscle, as well as in all the other areas.
Parasympathetic (Vagal) Stimulation Slows the Cardiac Rhythm and Conduction.
Stimulation of the parasympathetic nerves to the heart (the vagus nerve) causes acetylcholine to be released at the vagal endings – you already know this!
This neurotransmitter has two major effects on the heart.
First, it decreases the rate of rhythm of the sinus node, and second, it decreases the excitability of the A-V junctional fibers between the atrial musculature and the A-V node, thereby slowing transmission of the cardiac impulse into the ventricles.
Weak to moderate vagal stimulation slows the rate of heart pumping, often to as little as one-half normal.
Furthermore, strong stimulation of the vagi can completely stop the rhythmical excitation by the sinus node or completely block transmission of the cardiac impulse from the atria into the ventricles through the A-V node.
In either case, rhythmical excitatory signals are no longer transmitted into the ventricles.
The ventricles may stop beating for 5 to 20 seconds, but then some small area in the Purkinje fibers, usually in the ventricular septal portion of the A-V bundle, develops a rhythm of its own and causes ventricular contraction at a rate of 15 to 40 beats per minute.
This phenomenon is called ventricular escape.
Mechanism of the Vagal Effects.
The acetylcholine released at the vagal nerve endings greatly increases the permeability of the fiber membranes to potassium ions, which allows rapid leakage of potassium out of the conductive fibers.
This process causes increased negativity inside the fibers, an effect called hyperpolarization, which makes this excitable tissue much less excitable.
In the sinus node, the state of hyperpolarization makes the resting membrane potential of the sinus nodal fibers considerably more negative than usual—that is, −65 to −75 millivolts rather than the normal level of −55 to −60 millivolts.
Therefore, the initial rise of the sinus nodal membrane potential caused by inward sodium and calcium leakage requires much longer to reach the threshold potential for excitation.
This requirement greatly slows the rate of rhythmicity of these nodal fibers.
If the vagal stimulation is strong enough, it is possible to stop the rhythmical self excitation of this node entirely.
Sympathetic Stimulation Increases the Cardiac Rhythm and Conduction
It increases the rate of sinus nodal discharge.
It increases the rate of conduction, as well as the level of excitability in all portions of the heart.
It increases greatly the force of contraction of all the cardiac musculature, both atrial and ventricular
In short, sympathetic stimulation increases the overall activity of the heart.
Maximal stimulation can almost triple the heartbeat frequency and can increase the strength of heart contraction as much as twofold.
Mechanism of the Sympathetic Effect.
Stimulation of the sympathetic nerves releases norepinephrine at the sympathetic nerve endings (you already know this!).
Norepinephrine, in turn, stimulates beta-1 adrenergic receptors, which mediate the effects on heart rate
This increases the permeability of the fiber membrane to sodium and calcium ions.
In the A-V node and A-V bundles, increased sodium calcium permeability makes it easier for the action potential to excite each succeeding portion of the conducting fiber bundles, thereby decreasing the conduction time from the atria to the ventricles.
The increase in permeability to calcium ions is at least partially responsible for the increase in contractile strength of the cardiac muscle under the influence of sympathetic stimulation
Heart Anatomy Review
Cone-shaped hollow muscular organ found in the mediastinum à space between the lungs in thoracic cavity.
In quadrupeds, the base of the heart (region where large blood vessels enter and exit the heart) is directed dorsally (superiorly) and the apex (pointed end) of the heart is directed ventrally (inferiorly).
Pericardium is the connective tissue sac that encloses the heart.
Consists of an outer fibrous pericardium and an inner serous pericardium
Functions of the fibrous pericardium include:
Preventing overstretching of the heart
Providing some protection for heart
Anchoring the heart into the mediastinum
The heart fits into the serous pericardium like "a fist pushed into a water balloon".
The serous pericardium is composed of two layers separated by a fluid-containing cavity.
The visceral layer (also called the epicardium) adheres to the myocardium or muscle of the heart
Between the two layers of the serous pericardium is the pericardial cavity, a space containing pericardial fluid that lubricates and reduces friction between the two pericardial membranes as the heart contracts and relaxes.
The wall of the heart is composed of three layers:
Epicardium (visceral layer of serous pericardium) à connective tissue layer on the outer surface of heart.
Myocardium -> thick layer of cardiac (striated, involuntary) muscle that makes up the bulk of the mass of the heart.
Responsible for the heart's pumping ability.
Endocardium is the innermost layer
Heart chambers
Two (Right and left) upper atria (entry hall) collect blood from the veins and then pump it into the ventricles.
Each atrium has an auricle which is a small earlike extension on the cranial (anterior) side of the heart that increases the volume of the chambers.
Two (right and left) lower ventricles (little belly) that do most of the pumping of the blood out to the tissues of the body.
The two ventricles are separated by a thick muscular septum called the interventricular septum.
Heart valves are composed of connective tissue covered by endothelium.
Valves prevent backflow of blood between various heart chambers and thus ensure that blood flows in single direction through the heart.
The heart contains 4 valves:
Two atrioventricular (AV) valves are found between the atria and their corresponding ventricles.
Tricuspid valve or Right AV valve is found between right atrium and right ventricle
Bicuspid (mitral) valve or Left AV valve is found between left atrium and left ventricle. This valve has two cusps or flaps.
Both are attached to chordae tendineae that are attached to papillary muscles -> Keep the cusps of the valves pointing in the direction of the blood flow -> prevent blood from moving from the ventricles back into the atria.
Two semilunar valves between the ventricles and large arteries exiting the heart. Both semilunar valves are tricuspid -> Prevent backflow of blood from the arteries back into the ventricles.
Pulmonary semilunar valve is found at junction of right ventricle and pulmonary artery.
Aortic semilunar valve is found at the junction of left ventricle and the aorta.
Cardiac cycle
Two main concepts: Systole and Diastole
Systole: When the cardiac muscle contracts, it can be atrial or ventricular. Functionally it is when either the atria or ventricles “expel” blood towards the ventricles, or lungs/body.
Diastole: When the cardiac muscle relaxes and dilates, it can be atrial or ventricular. Functionally it is when either the atria or ventricles receive blood.
When the ventricles are full of blood and ready to start contracting, the following events take place:
Period of Isovolumic (Isometric) Contraction.
Immediately after ventricular contraction begins, the ventricular pressure rises abruptly, causing the atrioventricular (A-V) valves to close.
An additional 0.02 to 0.03 second is required for the ventricle to build up sufficient pressure to push the semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery.
During this period, contraction is occurring in the ventricles, but no emptying occurs.
This period is called the period of isovolumic or isometric contraction, meaning that cardiac muscle tension is increasing but little or no shortening of the muscle fibers is occurring
Period of Ejection.
When the left ventricular pressure rises slightly above 80 mm Hg (and the right ventricular pressure rises slightly above 8 mm Hg), the ventricular pressures push the semilunar valves open.
Immediately, blood is ejected out of the ventricles into the aorta and pulmonary artery.
Approximately 60% of the blood in the ventricles at the end of diastole is ejected during systole
About 70% of this portion flows out during the first third of the ejection period, with the remaining 30% emptying during the next two thirds.
The first third is called the period of rapid ejection, and the last two thirds are called the period of slow ejection.
Period of Isovolumic (Isometric) Relaxation.
At the end of systole, ventricular relaxation begins suddenly, allowing both the right and left intraventricular pressures to decrease rapidly.
The elevated pressures in the distended large arteries that have just been filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed.
For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change, giving rise to the period of isovolumic or isometric relaxation.
During this period, the intraventricular pressures rapidly decrease back to their low diastolic levels.
Then, the A-V valves open to begin a new cycle of ventricular pumping
During ventricular systole, large amounts of blood accumulate in the right and left atria
because of the closed A-V valves. Therefore, as soon as systole is over, and the ventricular pressures fall to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles.
End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output
During diastole, in humans, normal filling of the ventricles increases the volume of each
ventricle to about 110 to 120 ml. This volume is called the end diastolic volume.
As the ventricles empty during systole, the volume decreases by about 70 ml, which is called the stroke volume output.
The remaining volume in each ventricle, about 40 to 50 ml, is called the end-systolic volume.
The fraction of the end-diastolic volume that is ejected is called the ejection fraction, usually equal to about 0.6 (or 60%).
The ejection fraction percentage is often used clinically to assess cardiac systolic (pumping) capability.
When the heart contracts strongly, the end-systolic volume may decrease to as little as 10 to 20 ml.
Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end-diastolic volumes can become as much as 150 to 180 ml in the healthy heart.
By both increasing the end-diastolic volume and decreasing the end-systolic volume, the stroke volume output can be increased to more than double that which is normal.
Graphic analysis of ventricular pumping
Phase I: Period of Filling.
Phase I begins at a ventricular volume of about 50 ml and a diastolic pressure of 2 to 3 mm Hg.
The amount of blood that remains in the ventricle after the previous heartbeat, 50 ml, is called the end-systolic volume.
As venous blood flows into the ventricle from the left atrium, the ventricular volume normally increases to about 120 ml, called the end-diastolic volume, an increase of 70 ml.
Phase II: Period of Isovolumic Contraction.
During isovolumic contraction, the volume of the ventricle does not change because all valves are closed.
However, the pressure inside the ventricle increases to equal the pressure in the aorta, at a pressure value of about 80 mm Hg.
Phase III: Period of Ejection.
During ejection, the systolic pressure rises even higher because of still more contraction of the ventricle.
At the same time, the volume of the ventricle decreases because the aortic valve has now opened, and blood flows out of the ventricle into the aorta.
Phase IV: Period of Isovolumic Relaxation.
At the end of the period of ejection the aortic valve closes, and the ventricular pressure falls back to the diastolic pressure level.
The ventricle returns to its starting point, with about 50 ml of blood left in the ventricle at an atrial pressure of 2 to 3 mm Hg
Heart sounds
The act of listening to sounds within the body is called auscultation, which is performed
using a stethoscope. The sound of a heartbeat comes primarily from turbulence in
blood flow caused by the closure of the valves, not from contraction of the heart
muscle.
First heart sound (LUBB) represents the closing of the atrioventricular valves soon after ventricular systole (contraction) begins.
Second sound (DUPP) represents the closing of the semilunar valves slightly after ventricular diastole (relaxation) begins.
Heart murmur - An abnormal heart sound usually consisting of a flow noise that is heard before or after the LUBB-DUPP or that may mask the normal sounds entirely.
Two potential causes of heart murmurs are:
Valvular insufficiency - the incomplete closing of the valves.
Valvular stenosis - the narrowing of the valves.
Not all murmurs are abnormal or symptomatic of disease
Circulatory routes
Two basic circulatory routes found in a mammal are:
Systemic circulation à system of vessels that carry oxygenated blood from left ventricle to the tissues (where it becomes deoxygenated) and then back to the right atrium.
Pulmonary circulation à system of blood vessels that carries deoxygenated blood from right ventricle to lungs (where it is oxygenated) and then back to the left atrium.
Systemic circulation
Cranial and caudal vena cava (Deoxygenated blood from tissues of the body – large systemic veins and coronary sinus) à right atrium of the heart à tricuspid valve à right ventricle à pulmonary semilunar valve à pulmonary artery à lungs where it is oxygenated.
Pulmonary circulation:
Lungs (Oxygenated blood flow) through pulmonary veins à left atrium à bicuspid valve à left ventricle à aorta semilunar valve à aorta (Distributed by the systemic circulatory route to the rest of the body)
As the blood circulates through the tissues of the body, it becomes deoxygenated and then returns to the right atrium through the venae cava.
Coronary circulation
System of blood vessels that serves the heart muscle
Oxygenated blood flows directly into the coronary arteries from the aorta.
Blood is carried in these arteries to various regions of the heart muscle.
Blood flows through capillaries serving the cardiac myofibers, where 02 is exchanged for C02.
Deoxygenated blood is collected by the coronary veins that drain into the coronary sinus and then into the right atrium.
Only the inner one-tenth millimeter of the endocardial surface can obtain significant nutrition directly from the blood inside the cardiac chamber
Most of the coronary venous blood flow from the left ventricular muscle returns to the right atrium of the heart by way of the coronary sinus.
The normal coronary blood flow in the resting person averages 70 ml/min/100 g of heart weight, or about 225 ml/min, which is about 4% to 5% of the total cardiac output.
During strenuous exercise, the heart in the young adult increases its cardiac output fourfold to sevenfold.
Coronary capillary blood flow in the left ventricle muscle is low during systole, which is opposite to flow in vascular beds elsewhere in the body.
The reason for this phenomenon is strong compression of the intramuscular blood vessels by the left ventricular muscle during systolic contraction.
During diastole, the cardiac muscle relaxes and no longer obstructs blood flow through the left ventricular muscle capillaries, so blood flows rapidly during all of diastole
Heart rate
Increasing Heart Rate Decreases Duration of the Cardiac Cycle.
When heart rate increases, the duration of each cardiac cycle decreases, including the contraction and relaxation phases (systole and diastole).
The duration of systole decreases, but not by as great a percentage as diastole.
Example: At a normal heart rate of 72 beats/min, systole comprises about 0.4 of the entire cardiac cycle. At three times the normal heart rate, systole is about 0.65 of the entire cardiac cycle.
This means that the heart beating very rapidly does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction.
Cardiac output
The amount of blood ejected by the left (or right) ventricle into the aorta (or pulmonary artery) per minute.
Most commonly it refers to the amount of blood pumped by the left ventricle to the body per minute.
Cardiac Output (CO; volume per minute) = Stroke Volume (SV; volume per beat) × Heart Rate (HR; beats/min)
CO = SV × HR / ↑stroke volume or ↑ heart rate = ↑ CO, and vice versa.
CO in average resting human is approximately 5 liters/min
The maximum percentage that CO can be increased above resting CO is called cardiac reserve.
CO can potentially be increased ≈5× resting CO, which would be 5 × 5 L/min = 25 L/min in vigorously exercising humans.
In horses, resting cardiac output is ≈13.5 L/min (HR = 30 bpm; SV = 450 mL/beat) and can increase to ≈300 L/min during vigorous activity in a Thoroughbred.
Arteries and Arterioles
The function of the arteries is to transport blood under high pressure to the tissues. For this reason, arteries have strong vascular walls, and blood flows at a high velocity in the arteries.
Arterioles are the last small branches of the arterial system; they act as control conduits through which blood is released into the capillaries. Arterioles have strong muscular walls that can close the arterioles completely or, by relaxing, can dilate the vessels severalfold; thus, arterioles can vastly alter blood flow in each tissue in response to its needs.
Capillaries and venules
The function of the capillaries is to exchange fluid, nutrients, electrolytes, hormones, and other substances between the blood and interstitial fluid. To serve this role, the capillary walls are thin and have numerous minute capillary pores permeable to water and other small molecular substances.
The venules collect blood from the capillaries and gradually coalesce into progressively larger veins.
Veins
The veins function as conduits for transport of blood from the venules back to the heart.
The veins also serve as a major reservoir of extra blood. Because the pressure in the venous system is low, the venous walls are thin. Even so, they are muscular enough to contract or expand and thereby serve as a controllable reservoir for the extra blood, either a small or a large amount, depending on the needs of the circulation.
Microcirculation
Each nutrient artery entering an organ branches six to eight times before the arteries become small enough to be called arterioles.
Then, the arterioles branch two to five times, reaching diameters of 5 to 9 micrometers at their ends, where they supply blood to the capillaries.
At the point where each true capillary originates from a metarteriole, a smooth muscle fiber usually encircles the capillary.
This structure is called the precapillary sphincter, and it can open and close the entrance to the capillary.
The venules are larger than the arterioles and have a much weaker muscular coat.
The pressure in the venules is much less than that in the arterioles.
The metarterioles and precapillary sphincters are in close contact with the tissues they serve.
The local conditions of the tissues—such as the concentrations of nutrients, end products of metabolism, and hydrogen ions—can cause direct effects on the vessels to control local blood flow in each small tissue area.
Blood flow in capillaries
Blood usually does not flow continuously through the capillaries. Instead, it flows intermittently, turning on and off every few seconds or minutes.
This happens because of the intermittent contraction of the metarterioles and precapillary sphincters (vasomotion).
Despite the fact that blood flow through each capillary is intermittent, so many capillaries are present in the tissues that their overall function becomes averaged.
Water and nutrient exchange between the blood and interstitial fluid
Diffusion through the capillary membrane is the most important means of transferring substances between plasma and interstitial fluid
As the blood flows along the lumen of the capillary, tremendous numbers of water molecules and dissolved particles diffuse back and forth through the capillary wall, providing continual mixing between the interstitial fluid and plasma.
Electrolytes, nutrients, and waste products of metabolism all diffuse easily through the capillary membrane.
Proteins are the only blood constituents that do not readily pass through the capillary membrane
Lipid-soluble substances diffuse directly through the cell membranes of the capillary endothelium
Such substances include oxygen and carbon dioxide
Intercellular cleft: thin-slitted, curving channel that lies between adjacent endothelial cells.
The width of the capillary intercellular cleft pores, 6 to 7 nanometers, is about 20 times the diameter of the water molecule, which is the smallest molecule that normally passes through the capillary pores.
The diameters of plasma protein molecules, however, are slightly greater than the width of the pores.
Other substances, such as sodium ions, chloride ions, glucose, and urea, have intermediate diameters.
The permeability of the capillary pores for different substances varies according to their molecular diameters
The size of the pores varies greatly depending on the tissue
In the brain, the junctions between the capillary endothelial cells are tight junctions that allow only extremely small molecules such as water, oxygen, and carbon dioxide to pass into or out of the brain tissues.
In the liver, the clefts between the capillary endothelial cells are nearly wide open so that almost all dissolved substances of the plasma, including the plasma proteins, can pass from the blood into the liver tissues.
The pores of the gastrointestinal capillary membranes are midway in size between those of the muscles and those of the liver.
In the glomerular capillaries of the kidney, numerous small oval windows called fenestrae penetrate all the way through the middle of the endothelial cells so that tremendous amounts of small molecular and ionic substances (but not the large molecules of the plasma proteins) can filter through the glomeruli without having to pass through the clefts between the endothelial cells
Fluid filtration across capillaries
The hydrostatic pressure in the capillaries tends to force fluid and its dissolved substances through the capillary pores into the interstitial spaces.
Conversely, osmotic pressure caused by the plasma proteins (colloid osmotic pressure) tends to cause fluid movement by osmosis from the interstitial spaces into the blood.
This osmotic pressure exerted by the plasma proteins normally prevents significant loss of fluid volume from the blood into the interstitial spaces
Net exchange pressure across capillary walls at any point in a capillary can be determined using the following equation referred to as the Starling Hypothesis:
Net exchange pressure = (PC + πIF) – (PIF + πP)
Where:
PC = Capillary hydrostatic pressure
PIF = Interstitial fluid hydrostatic pressure
πP = Plasma colloid osmotic pressure
πIF = Interstitial colloid osmotic pressure
(PC + πIF) represents the net outward driving pressures.
(PIF + πP) represents the net inward driving pressures.
Hydrostatic Pressure
Pressure exerted on vessels walls by fluid (blood – “outward” or interstitial fluid – “inward”)
Net filtration pressure (NFP) = PC – PIF
Capillary hydrostatic pressure (PC) is the blood pressure in the capillary bed. It varies depending on arterial pressure, venous pressure, precapillary and post-capillary resistance.
In general, PC is highest on the arteriolar end of the capillary bed (37 mm Hg) and lowest on the venular end (17 mm Hg).
Interstitial fluid hydrostatic pressure (PIF) is extremely low (≈1 mm Hg) throughout the capillary bed under normal conditions.
Colloid Osmotic (Oncotic) Pressure
Osmotic pressure created by the presence of non-filterable proteins in the plasma.
Plasma colloid osmotic pressure (πP) = 25 mm Hg.
Interstitial colloid osmotic pressure (πIF) = 0 mm Hg.
Note: Other than proteins, most solutes (like ions and small molecules) diffuse easily between plasma and IF, and therefore do not contribute to colloid osmotic pressure.
So, using net exchange pressure to determine net direction of bulk flow at the both ends of a capillary bed:
Net exchange pressure = (PC + πIF) – (PIF + πP)
Net exchange under normal conditions:
On the arteriolar end of capillary bed:
Net exchange pressure = (37 + 0) – (1 + 25) = +11 mm Hg
The positive net exchange pressure means that ultrafiltration is occurring on the arteriolar end of the capillary bed.
On the venular end of capillary bed:
Net exchange pressure = (17 + 0) – (1 + 25) = -9 mm Hg
The negative net exchange pressure means that reabsorption is occurring on the venular end of the capillary bed.
Note: In most capillary beds, net ultrafiltration (capillary to interstitial space) is greater than net reabsorption (interstitial space to venule) resulting in accumulation of fluid in the interstitial space. On average, ultrafiltration from all capillary beds in humans exceeds reabsorption by about 3 liters/day or about 9/10 of what was filtered in the capillaries is reabsorbed in the venules. This non-absorbed fluid is “picked up” by the lymphatic system. (More on this later!)
Abnormal imbalance of forces at the capillary membrane
If the mean capillary pressure rises significantly above the average value of 17 mm Hg, the net force tending to cause filtration of fluid into the tissue spaces rises.
Fluid will begin to accumulate in the interstitial spaces and edema will result
Conversely, if the capillary pressure falls very low, net reabsorption of fluid into the capillaries will occur instead of net filtration, and the blood volume will increase at the expense of the interstitial fluid volume.
Edema
Excessive accumulation of interstitial fluid in the interstitial spaces within a tissue.
Example: pulmonary edema is excess accumulation of fluid in the interstitial spaces of the lungs.
Edema may result for a variety of reasons. Some common causes include:
High arterial blood pressure, Blood volume (pregnancy).
Venous obstruction.
Leakage of plasma proteins into interstitial fluid.
Loss of plasma proteins in the urine due to leakage of plasma proteins into filtrate in the renal corpuscle of the kidney.
Decreased plasma protein concentration due to severe starvation or liver failure.
Kwashiorkor is a form of severe protein malnutrition observed in malnourished children.
One sign of this disease is a severely swollen belly, which is primarily due to fluid accumulation in the peritoneal cavity (ascites = peritoneal edema).
This form of edema results from lower concentration of plasma proteins and the corresponding lower plasma colloid osmotic pressure (πP).
Obstruction of lymphatic drainage = Lymphedema.
Lymphatic system
The lymphatic system represents an accessory route through which fluid can flow from the interstitial spaces into the blood.
Most importantly, the lymphatics can carry proteins and large particulate matter away from the tissue spaces, neither of which can be removed by absorption directly into the blood capillaries.
This return of proteins to the blood from the interstitial spaces is an essential function, without which the animal would die within about 24 hours.
Lymphatic System – Three general functions:
Transports excess interstitial (tissue) fluid back into the bloodstream.
Transports absorbed fat from small intestine to the bloodstream.
Help provide immunological defenses against pathogens in lymphatic tissues like lymph nodes, tonsils, and spleen.
Lymphatic vessels are found in all tissues except cartilage, bone, epithelium, and CNS tissues.
The smallest vessels of the lymphatic system are the lymphatic capillaries, which are closed-ended vessels found widely dispersed in the capillary beds of most tissues.
Lymphatic capillaries are highly permeable to almost all dissolved chemicals (along with particulates, microbes, and cells).
Once interstitial fluid containing its solutes, microbes, cells, and particulates enters the lymphatic capillaries, it is referred to as lymph.
Lymphatic capillaries merge to form successively larger lymph vessels called lymphatics.
As the lymph moves through these vessels, it circulates through lymph nodes, which are oval or kidney-shaped organs that act as lymph filters to remove foreign particles like bacteria and viruses and to help orchestrate immune responses to pathogens.
The lymphatics eventually merge into the right and left thoracic ducts that drain into the subclavian veins near where these veins connect with the internal jugular vein.
Lymphatics contain a system of one-way valves and movement of lymph is driven by skeletal muscle pumping, lymphatic vessel smooth muscle contractions, and tissue pressure.
There is no dedicated pump for lymph circulation in mammals.
Throughout the course of the day, flow of lymph varies considerably.
It is highest during exercise and lowest during periods of inactivity.
Lymphatic system circulation
Average lymph flow per day is about equal to the animal’s volume of plasma (3 liter/day in humans).
Lymphedema results from blockage of the lymphatics leading to edema in the most compliant tissues (usually subcutaneous) in the area of the body where the blockage occurs.
Example: Elephantiasis is an example of what happens during severe lymphatic blockage. It is caused by the larvae of the filariasis worm, which invade and block the lymphatic system causing massive lymphedema in extremities and other soft tissues.
The fluid that returns to the circulation by way of the lymphatics is extremely important because substances of high molecular weight, such as proteins, cannot be absorbed from the tissues in any other way.
At the junctions of adjacent endothelial cells, the edge of one endothelial cell overlaps the edge of the adjacent cell in such a way that the overlapping edge is free to flap inward, thus forming a minute valve that opens to the interior of the lymphatic capillary.
However, this fluid has difficulty leaving the capillary once it has entered because any backflow closes the flap valve
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