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The heart

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The heart Powered By Docstoc
					Silverthorn Chapter 14: Cardiovascular
Physiology.                       3/25/2008 5:56:00 PM
 - The heart:
    (a) septum
        - The septum is what divides the heart into the left and right halves.
        - Each half functions as an independent pump.
        - the right side of the heart receives deoxygenated blood from the
          tissues and pumps it to the lungs to gain oxygen.
        - The left side of the heart receives newly oxygenated blood from the
          lungs and pumps it to the rest of the body.
        [Although blood is often described as deoxygenated, it is not
        completely devoid of oxygen, it just has less oxygen than the blood
        that is being sent to the rest of the body.]
    (b) atrium
        - Both halves of the heart have an atrium.
        - The atrium receives blood returning to the heart from the body.
    (c) ventricle
        - Both halves of the heart also have a ventricle.
        - The ventricle pumps blood out to the body via blood vessels.
     (d) apex of the heart is the pointed bottom portion that is angled
         downward toward the left side of the body.
     (e) base the broader top portion. Lies behind the sternum.
     (f) pericardium is membrane sac that surrounds the heart.
     (g) pericardial fluid is found in a thin clear layer between the outside
         of the heart and the pericardium. This fluid lubricates the surface
         of the heart as it beats to reduce friction.


 myocardium is also known as cardiac muscle and is what the heart is mostly
 composed of. The myocardium is covered by thin outer and inner layers of
 epithelium and connective tissue.


 - The pathway of blood:
    (1) Blood flows from the right atrium to the right ventricle. The
        right ventricle pumps the blood to the lungs via the
        pulmonary arteries to be oxygenated.
    (2) Blood leaves the lungs and enters the left atrium via pulmonary veins.
        Pulmonary circulation refers to the blood vessels that go from the
       right ventricle to the lungs and back to the left atrium.
   (3) The blood is pumped out of the left ventricle and into the aorta.
       The aorta branches into smaller and smaller arteries that eventually
       lead to a network of capillaries.
   (4) Blood leaves the capillaries and enters the venous side of
       circulation, moving from small veins to larger and larger ones.
       The veins at the upper part of the body join together to form the
       superior vena cava. Veins from the lower half of the body join
       to create the inferior vena cava.
       Both the superior and the inferior vena cava empty into the right
       atrium.
       Systemic circulation refers to the blood vessels that carry blood from
       the left side of the heart to the tissues and back to the right side.


Valves. Location and structure and function:
Blood flows from the veins into the atria and from there into the ventricles.
In order to reach the ventricles, the blood must flow through one-way valves.
Similarly, when blood leaves the heart from the ventricles, it must pass
through a second set of valves. Therefore, the ventricles contract fro mthe
bottom up in order for blood to be squeezed out the top.


Each valve is surrounded by rings made out of connective tissue. The rings
form the origin and insertion for the cardiac muscle, an arrangement that
pulls the apex and base together when the ventricles contract. The connective
tissue also acts as an electrical insulator, blocking most transmission of
electrical signals between the atria and ventricles.
This arrangement ensures that the electrical signals can be directed through
a specialized conduction system to the apex of the heart for the bottom to
top contraction.


The valves ensure one-way flow of blood.
There are two sets of two valves:
   (a) atrioventricular valves
          - located between the atria and the ventricles.
          - formed from thin flaps of tissue joined at the base to a
            connective tissue ring.
          - the flaps are slightly thicker on the edge
          - chordae tendineae are the collagenous tendons that the flaps
            connect to on the ventricular side of the valve.
            Chordae tendineae precent the valve from being pushed back into
            atrium when a ventricle contracts.
            [if the chordae fail, it is a condition called 'prolapse]
          - papillary muscles are mound-like extensions of ventricular
            muscle and provide stability for the chordae tendineae.
          - Neither the papillary muscles nor the chordae tendineae actively
            open the valve. [The valve passively opens when flowing blood
            pushes on the flaps.
          - tricuspid valve is the valve separating the right atrium and the
            right ventricle.
            This valve has three flaps.
          - Bicuspid valve has two flaps and separates the left atrium and
            the left ventricle. [this valve is also called the mitral valve]
    (b) semilunar valves
          - located between the ventricles and the major arteries.
          - aortic valve separates the aorta and the left ventricle.
          - pulmonary valve separates the right ventricle and the
            pulmonary trunk.
          - both of the semilunar valves have three flaps.
          - Neither of the valves are connected to tendons as the
            atrioventricular valves are.


[One part of the aorta branches off into coronary arteries supply the heart
muscle with blood. The blood from the coronary arteries travels into
capillaries and then into coronary veins which empty directly into the right
atrium at the coronary sinus.
Ascending branches of the aorta go to the head, brain and arms.
The abdominal aorta brings blood to the trunk legs and internal organs.]


- Blood flows because liquids and gases flow down pressure
                        gradients.
[Blood can only flow in a cardiovascular system if one region is of higher
presser than the other regions.]


In humans high pressure is created by the contraction of the ventricles.
This pressure causes the blood to flow out of the heart into the blood
vessels [the region of low pressure].
As the blood flows through the blood vessels pressure is lost because of the
friction between the blood and the walls of the blood vessels.
Therefore, pressure continuously decreases as blood gets farther and farther
away from the heart.


The highest pressure in the vessels of the cardiovascular system is found in
the aorta and systemic arteries as they receive blood from the left
ventricle.
The lowest pressure is in the vena cavae just before they empty into the
right atrium.


- Pressure in a fluid is the force exerted by the fluid on its surroundings.
- Hydrostatic pressure refers to the force a fluid exerts on its surroundings
  when the fluid is not moving and force is exerted equally in all directions


[In the heart and blood vessels pressure is usually measured in mm Hg]


The pressure exerted by moving fluid has two components:
   (a) dynamic, flowing component:
       Represents the kinetic energy of the system.
   (b) lateral component:
       Represents the hydrostatic pressure [potential energy] exerted on the
       walls of the system.


- Velocity of flow depends on the flow rate and the cross sectional area.
   - flow usually refers to flow rate which is the volume of blood that
     passes a given point in the system per unit time.
     [When referring to circulation, flow is either expressed in L/min or in
     mL/min.]
  - velocity of flow is the distance a fixed volume of blood travels in a
    given period of time.
    Velocity of flow measures how fast blood flows past a point.


The relationship between velocity of flow, flow rate, and cross sectional
              area of the tube is expressed by the equation:


                              v= Q/A

                      When: v = velocity of flow
                            Q = flow rate
                            A= cross sectional area of the tube.


  - In a tube with a fixed diameter
    [and thus a fixed cross sectional area], the velocity of flow
    is directly related to flow rate.
  - In a tube whose diameter varies the velocity of flow varies inversely
    with the diameter [so long as the flow rate is constant].
    [Velocity is faster in narrow sections and slower in wider sections.]


Arteries act as a pressure reservoir when the heart is in a relaxed state.
Arteries exert pressure to keep the driving force of blood circulating when
the heart is at rest [not exerting any pressure] in order to keep bloow
flowing.
This pressure is called the mean arterial pressure [MAP] and is influenced by
two things:
  (a) cardiac output: the volume of blood the heart pumps per minute.
  (b) peripheral resistance: the resistance of the blood vessels to the
      blood flowing through them.


[mean arterial pressure] is proportional to [cardiac output]x[ p. resistance]


- Cardiac muscle cells contract without nervous stimulation.
The heart is made of myocardium [cardiac muscle cells] which mostly is
contractile. But about 1% of myocardial cells generate action potentials
spontaneously - giving the heart unique ability to contract without any
outside signal. The heart can contract without any connections to the rest of
the body because the signal for contraction is myogenic, it originates within
the heart muscle itself.


- Cardiac muscle differs from skeletal muscle but shares similarities with
                               smooth muscle.
   (a) Cardiac muscle fibers are much smaller than skeletal muscle fibers
       and usually only have one nucleus per fiber.
   (b) Individual cardiac muscle cells branch and join neighboring cells
       end-to-end to create a complex network.
       Intercalated disks are the cell junctions and consist of intercalated
       membranes. These disks have two components:
           . desmosomes: strong connections that tie adjacent cells together.
             this allows the force created in one cell to be transferred
             to the adjacent cell.
           . gap junctions.
   (c) Gap junctions in the intercalated disks electrically connect cardiac
       muscle cells together which allows waves of depolarization to spread
       rapidly from cell to cell. Therefore, almost all of the heart muscle
       cells contract simultaneously.
   (d) t-tubules of myocardial cells are larger than those of skeletal muscle
       muscle, and they branch inside the myocardial cells.
   (e) myocardial sarcoplasm reticulum is smaller than that of skeletal
       muscle, because cardiac muscle depends on extracellular Ca2+
       to initiate contraction. [In this respect, cardiac muscle resembles
       smooth muscle.]
   (f) Mitochondria occupy about one third the cell volume of a cardiac
       contractile fiber, a reflection of the high energy demand of these
       cells. Cardiac muscle consumes between 70 and 80% of the oxygen
       delivered by the blood. This is more than twice the amount consumed
       by other cells in the body.




- autorhythmic cells
   - [or 'pace makers'] are the cells responsible for releasing the signal
     for contraction.
   - Autorhythmic cells set the rate of the heartbeat.
   - They are smaller and contain few contractile fibers compared to
     contractile cells.
   - Do not contribute to the contractile force of the heart because they do
     not have organized sarcomeres.


- contractile cells
   - typical striated muscle, but have contractile fibers organized into
     sarcomeres.


Cardiac excitation-contraction coupling combines features of skeletal and
                             smooth muscle.


In cardiac muscle, an action potential initiates EC coupling, but the action
potential originates spontaneously in the hearts pacemaker cells and spreads
into the contractile cells through gap junctions.
An action potential that enters a contractile cell moves across the
sarcolemma and into the t-tubules, where it opens voltage-gated Ca2+ channels
in the cell membrane. Ca2+ enters the cell and opens ryanodine receptor-
channels [which are operated by Ca2+ binding]    in the sarcoplasmic reticulum.


Ryanodine receptor-channels are Ca2+ channels.
   when they are open there is a Ca2+ - induced Ca2+ release. Stored Ca2+
   flows out of the sarcoplasmic reticulum into the cytosol which creates
   a Ca2+ 'spark'.


Calcium released from the sarcoplasmic reticulum provides about 90% of the
calcium needed for muscle contraction.
Calcium diffuses through the ctyosol to the contractile elements, where the
ions bind to troponin and initiate the cycle of crossbrdige formation and
movement. Contraction takes place by the same type of sliding filament
movement that occurs in skeletal muscle.


Relaxation in cardiac muscle is similar to the relaxation of skeletal
muscles. As cytoplasmic Ca2+ concentrations decrease, Ca2+ unbinds from
troponin, myosin releases actin, and the contractile filaments slide back to
their relaxed position. Ca2+ is transported back into the sarcoplasmic
reticulum via Ca2+ = ATPase. Ca2+ is also removed from the cell in exchange
for Na+ via a Na+ - Ca2+ antiport protein. [Each Ca2+ moves out of the cell
against its electrochemical gradient in exchange for 3 Na+ entering the cell
down their concentration gradient.]


- Cardiac muscle contraction can be graded.
A single muscle fiber can vary the amount of force it generates, as opposed
to skeletal muscle in which contraction in a single fiber is all-or-none at
any given fiber length. The force generated by cardiac muscle is proportional
to the number of crossbridges that are active. the number of active
crossbridges is determined by how m uch Ca2+ is bound to troponin.
If cytosolic Ca2+ concentrations are low, some crossbridges will not be
activated and contraction force will be small. if additional Ca2+ enters the
cell from the extracellular fluid, more Ca2+ is released from the
sarcoplasmic reticulum. This additional Ca2+ binds to troponin which enhances
the ability of myosin to form crossbridges with actin and therefore creating
additional force.


- When cardiac muscle is stretched, it contracts more forcefully.
A factor that affects the force of contraction in cardiac muscle is the
sarcomere length at the beginning of contraction. For both cardiac and
skeletal muscle, the tension generated is directly proportional to the
initial length of the muscle fiber.
As muscle fiber length and sarcomere length increase, tension increases up to
a maximum.


- Action potentials in myocardial cells vary according to cell type.
Cardiac muscle is an excitable tissue with the ability to generate action
potentials. Each of the two types of cardiac muscle has a different action
potential, but Ca2+ plays an important role in both.
  myocardial contractile cells
   (a) Phase 4: resting membrane potential.
        - myocardial contractile cells have a stable resting potential of
             about -90 mV.
   (b) Phase 0: depolarization.
        - When a wave of depolarization moves into a contractile cell through
        gap junctions, the membrane potential becomes more positive.
        Voltage-gated Na+ channels open, Na+ enters the cell and rapidly
        depolarizes it.
      - The membrane potential reaches about +20 mV before the Na+
        channels close.
 (c) Phase 1: initial repolarization.
      - When the Na+ channels close, K+ leaves through open K+ channels
        and the cell begins to repolarize.
      - this phase is very brief.
 (d) Phase 2: the plateau.
      - Two events occur which causes the action potential to flatten:
        event 1: K+ permeability decreases. [K+ channels close]
        event 2: Ca2+ permeability increases.
      - Voltage-gated Ca2+ channels activated by depolarization have been
        slowly opening during phases 0 and 1.
        When they finally open, Ca2+ enters the cell, which lengthens the
        total duration of a myocardial action potential. [about 200 msec or
        more compared to 1-5 msec in a neuron or skeletal muscle tissue.]
      - The combination of Ca2+ entering and K+ leaving causes the action
        potential to flatten out into a plateau.
 (e) Phase 3: rapid repolarization.
      - Ca2+ channels close and K+ permeability increases and the plateau
        ends. The K+ channels in this phase are activated by depolarization
        but are slow to open. When they finally do open, K+ exits quickly
        and the cell returns to its resting potential.


   [The longer myocardial action potential helps prevent the sustained
   contraction - tetanus - by ensuring that the refractory period and the
   contraction end almost simultaneously. Prevention of tetanus in the
   heart is important because cardiac muscles need to relax between
   contraction to allow the ventricles to fill with blood.]


myocardial autorhythmic cells
  - Generate action potentials spontaneously because they have an unstable
     membrane potential, which is referred to as a pacemaker potential. The
     membrane potential starts at -60 mV and slowly drifts upward to
     threshold. Whenever the pacemaker potential depolarizes to threshold
     the autorhythmic cell fires an action potential.
    - The pacemaker potential drifts because the autorhythmic cell contains
     channels that are permeable to both Na+ and K+ called If channels.
     At -60 mV the If channels are permeable to K+ and Na+/
    - When the If channels are open at negative membrane potentials, the Na+
     influx exceeds the K+ efflux and the cell slowly depolarizes.
    - As Na+ concentration inside the cell becomes more positive, the If
     channels begin closing and some Ca2+ channels open. This continues the
     depolarization and the membrane potential continues to move toward
     threshold.
    - When the membrane potential reaches threshold, additional Ca2+ channels
     open and calcium rushes into the cell. This creates the steep
     depolarization phase of the action potential. [This is different than
     most excitable cells, which use Na+ channels during the
     depolarization phase.]
   - At the peak of the potential, Ca2+ channels close and slow K+ channels
    have opened. The repolarization phase of the autorhythmic action
    action potential is due to K+ leaving the cell.


- Autonomic neurotransmitters modulate heart rate.
Heart rate is determined by the speed with which pacemaker cells depolarize.
     Increased depolarization speed  increased heart rate
     Decreased depolarization speed  decreased heart rate


The interval between action potentials can be modified by altering the
permeability of the autorhythmic cells to different ions.
    (a) Increased permeability to Na+  speeds up depolarization
    (b) increased permeability to Ca2+  speeds up depolarization
    (c) Decreased permeability to Ca2+  slows depolarization
    (d) Increased permeability to K+  slows depolarization
       [because the pacemaker potential begins at a more negative value]
Sympathetic stimulation of pacemaker cells speeds up heart rate.
Catecholamines [norepinephrine and epinephrine] increase ion flow through
both If and Ca2+ channels. More rapid cation entry speeds up the rate of the
pacemaker depolarization, causing the cell to reach threshold faster and
increasing the rate of action potential firing, thus increasing heart rate.
Catecholamines bind to and activate the beta-adrenergic receptors on the
autorhythmic cell. The beta-receptors use a camp second messenger system to
alter the transport properties of the ion channels. In the case of the If
channels, camp itself is the messenger. When camp binds to open If channels,
they remain open longer.


The parasympathetic neurotransmitter acetylcholine slows heart rate by
activating muscarinic cholinergic receptors that influence K+ and Ca2+
channels in the pacemaker cell. K+ permeability increases and Ca2+
permeability of the pacemaker decreases. The combination of these two events
causes the cell to take longer to reach threshold, therefore, slowing heart
rate.


- The heart as a pump: electrical conduction in the heart coordinates
                              contraction.
Individual myocardial cells must depolarize and contract in a coordinated
fashion to make the heart contract with enough force to circulate blood.


Electrical communication in the heart:
  (1) Begins with an action potential in an autorhythmic     cell. The
        depolarization spreads to adjacent cells through gap junctions
        in the intercalated disks.
  (2) The depolarization wave is followed by a wave of contraction.
  (3) The wave of contraction passes across the atria and then reaches the
        ventricles.


The same thing as above, but in greater detail!
  (1) The depolarization begins in the sinoatrial node [SA node}.
        The SA node is a node of autorhythmic   cells in the right atrium
        that serve as the main pacemaker of the heart.
  (2) The depolarization wave spreads through a conducting system of
      noncontractile autorhythmic    fibers called the internodal pathway.
      The internodal pathway connects the SA node to the atrioventricular
      node [AV node].
      The AV node is a group of autorhythmic   cells on the bottom of the
      right atrium.
  (3) The depolarization wave moves from the AV node to the Purkinje fibers,
      specialized conducting cells that transmit electrical signals at very
      rapid rates.
      The Purkinje fibers are found in the atrioventricular bundle
      [AV bundle] which is located in the septum between the ventricles.
  (4) Going down the septum, the AV bundle fibers divide into left and right
      bundle branches. The bundle branch fibers continue downward to the apex
      where they divide into smaller Purkinje fibers that spread outward
      among the contractile cells.


The electrical signal for contraction begins when the SA node fires an action
potential and the depolarization spreads to adjacent cells through gap
junctions. Electrical conduction is rapid through the internodal conducting
pathways, but slower through the contractile cells of the atria.
As action potentials spread across the atria they reach the fibrous skeleton
of the heart at the junction of the atria and ventricles. This barricade
prevents the transfer of electrical signals from the atria to the ventricles.
therefore, the AV node is the only pathway through which action potentials
can reach the contractile fibers of the ventricles.
The electrical signal passes from the AV node through the AV bundle and
bundle branches to the apex of the heart. the Purkinje fibers transmit
impulses rapidly [4 m/s] which ensures that all contractile cells in the apex
contract nearly simultaneously.


Electrical signals MUST be directed through the AV node because and not
spread downward from the atria BECAUSE:
If electrical signals from the atria were conducted directly into the
ventricles, the ventricles would start contracting at the top and blood would
be squeezed downward and become trapped!


A second function of the AV node:
Slightly delay the transmission of action potentials in order to allow the
atria to complete their contraction before ventricular contraction begins.
The AV mode delay is accomplished by slowing conduction through the nodal
cells.


- Pacemakers set the heart rate
The cells of the SA node set the pace of the heartbeat.
The Purkinje and the AV node have unstable resting potentials and can
therefore also act as pacemakers under some conditions, but since their
rhythm is much slower than that of the SA node, they usually do not set the
pace for heartbeat.


If the SA node is damaged one of the slower pacemakers in the heart takes
over. It is possible for different parts of the heart of follow different
pacemakers.


-Electrocardiogram reflects the electrical activity of the heart
- The electrocardiogram [or ECG] provides indirect information
  about heart function.


  There are three main components of an ECG:
         (a) Waves: deflections above or below the baseline.
              - A positive deflection  an electrical wave moving
                through the heart is going toward a positive
                electrode.
              - A negative deflection  an electrical wave moving
                through the heart is going toward a negative
                electrode.
         (b) segments: sections of baseline between waves.
         (c) Intervals: combination of waves and segments.


  Three major waves can be seen on a normal ECG recorded from
  lead I:
         (a) P wave. is the first wave and corresponds to
              depolarization of the atria.
         (b) QRS Complex is a trio of waves that follows the P
             wave. This trio represents the progressive wave of
             ventricular depolarization.
             Atrial repolarization is not represented by a
             specific wave, but it is incorporated into the
             QRS complex.
       (c) T wave represents the repolarization of the
             ventricles.


  The father of the modern ECG was Walter Einthoven, who also
  created 'Einthoven's Triangle'.
- Einthoven's Triangle is a hypothetical triangle created by
  placing electrodes on both arms and the left leg.
  The sides of the triangle are numbered to correspond to three
  leads [A lead is a pair of electrodes] used for recording.
- An ECG is recorded from one lead at a time. One electrode acts
  as the positive electrode of the lead and the second electrode
  acts as the negative.
  [Example: In lead I the left arm electrode is positive and the
  right arm electrode is negative.]


An ECG tracing shows the summed electrical potentials generated by all cells
of the heart. Different components of the ECG reflect depolarization or
repolarization of the atria and ventricles.
Because depolarization initiates muscle contraction, these electrical events
of an ECG can be associated with contraction or relaxation, which are
mechanical events.


-The cardiac cycle [a single contraction-relaxation cycle]
The mechanical events of a cardiac cycle lag behind the electrical signals.
Therefore:
  - Atrial contraction begins during the latter part of the P
    wave and continues during the PR segment.
  - Ventricular contraction begins just after the Q wave and
    continues through the T wave.


- Interpreting an ECG:
  (a) Heart rate:
    - Heart rate is normally timed either from the beginning of
         one P wave to the beginning of the next P wave or from the
         peak of one R wave to the peak of the next R wave.
  (b) if one or more P waves occurs without a following QRS
         complex, a condition of heart block may be present.


- The heart contracts and relaxes once during a cardiac cycle
Each cardiac cycle has two phases:
(a) diastole: the time when cardiac muscles relax.
(b) systole: the time when the muscle is contracting.


  (1) The heart at rest: atrial and ventricular diastole
         The cardiac cycle begins with both the atria and the ventricles
         relaxed. At this time:
         Atria  filling with blood from the veins.
         Ventricles  just finished a contraction.
         AV valves  open
         Blood flows from the atria into the ventricles.
  (2) Completion of ventricular filling: atrial systole contraction of atria
         - The last 20% of filling of the ventricles occurs when the atria
           contract and push blood into the ventricles.
     -     The ventricles now contain the maximum volume of blood they will ever
           hold in the cycle. Because this maximum filling occurs at the end of
           the ventricular relaxation [diastole] it's called the
           end-diastolic-volume [EDV].
     -     When the atria contract a small amount of blood is pushed back into
           the veins because there is no valve to prevent backflow. [This can be
           observed as a pulse in the jugular vein.]
  (3) Early ventricular contraction and the first heart sound
         As the atria are contracting, the depolarization wave is moving
         slowly through the conducting cells of the AV node, then quickly down
         the Purkinje fibers to the apex of the heart.
         Ventricular systole begins there. Blood pushing against the underside
         of the AV valves forces them closed so that blood can not flow back
         into the atria.
      Vibrations following the closure of the AV valve creates the
      'first heart sound' of a heartbeat.
      While the ventricles begin to contract the atria are repolarizing and
      relaxing. When atrial pressure falls below venous pressure, blood flows
      from the veins into the atria again.
  (4) The heart pumps: ventricle ejection
      As the ventricles contract they generate enough pressure to open the
      semilunar valves and push blood into the arteries.
      During this phase the AV valve remains closed and the atria continue to
      fill.
      During this phase the ventricles contain the minimum amount of blood
      and this minimum volume is the end-systolic-volume [ESV]
  (5) Ventricular relaxation and the second heart sound.
      - At the end of ventricular ejection the ventricles begin to repolarize
        and relax - thus making the ventricular pressure decrease. When it
        decreases below arterial pressure the semilunar valves close, cued by
        the back pushing of blood. The closing of these valves is called the
        'second heart sound'.
      - Isovolumic ventricular relaxation: a period of time when the volume
        of blood in the ventricles is not changing. Ventricular pressure is
        decreasing, but it is still higher than atrial pressure.
      - When ventricular relaxation causes ventricular pressure to become
        less than atrial pressure the AV valves open and the blood that has
        been accumulating in the atria rushes into the ventricles and the
        cycle starts over.


 - Pressure - volume curves represent one cardiac cycle.
A pressure - volume graph represents the changes in volume and pressure
during one cardiac cycle. [change in volume is the X-axis and change in
pressure is the Y-axis].


- Stroke volume is the volume of blood pumped by one ventricle in one
                             contraction.
Some blood remains in the ventricles at the end of each contraction to
provide a safety margin. With a more forceful contraction, the heart can
decrease its end systolic volume, sending additional blood to the tissues.
  - Stroke volume refers to the amount of blood pumped by one ventricle
    during a contraction. Stroke volume is measured in mL/beat and is
    calculated as follows:


    volume of blood before contraction-volume of blood after contraction = stroke volume.

                                    in other words:
                                 EDV - ESV = stroke volume



- Cardiac output is a measure of cardiac performance.
 Because all blood that leaves the heart flows through the tissues, cardiac
 output is an indicator of total blood flow through the body.


- Cardiac output is the volume of blood pumped by one ventricle in a given
  period of time. It is calculated using the following equation:


                   cardiac output = heart rate x stroke volume

 Normally cardiac output is the same for both ventricles, but if one fails
 the blood will pool in the circulation behind the weaker side of the heart.


  Homeostatic changes in cardiac output are accomplished by varying heart
  rate, stroke volume, or both. Cardiac output is altered by local and reflex
  mechanisms.


- Heart rate is modulated by autonomic neurons and catecholamines.
Although heart rate is initiated by autorhythmic             cells in SA node, it is
modulated by neural and hormonal input.


  Antagonistic control
     - the sympathetic and parasympathetic branches of the autonomic
       division influence heart rate through antagonistic control.
     - Parasympathetic activity slows heart rate.
     - Sympathetic activity increases heart rate.
     - Normally tonic control of heart rate is dominated by the
       parasympathetic branch.
     - When all sympathetic and parasympathetic input is blocked the
        spontaneous depolarization rate of the SA node is 90-100
        beats per minute. [This is called the intrinsic rate.]


  Two ways to increase heart rate:
    (1) decrease parasympathetic activity. As parasympathetic influence
        on the autorhythmic   cells decreases, the cells increase their
        depolarization rate to the intrinsic rate of 90-100 beats per minute.
    (2) Sympathetic input is needed to increase heart rate above the
        intrinsic rate.


- Multiple factors influence stroke volume.
 The force generated by cardiac muscle during a contraction is directly to
 stroke volume.


 The force of ventricular contraction is affected by:
   (a) the length of muscle fibers at the beginning of contraction.
       The length of the muscle is determined by the volume of blood in the
       ventricle at the beginning of contraction [EDV]
   (b) the contractility of the heart: the intrinsic ability to contract at
       any given fiber length. [Contractility is a function of Ca2+
       interaction with the contractile filaments.]


- Length-tension relationships and the Frank-Starling law of the heart
 - As sarcomere length increases contraction force increases.
 - As stretch of the ventricular wall increases, stroke volume increases.
 - If additional blood flows into the ventricles, the muscle fibers stretch
   and then contract more forcefully.


 - preload is the degree of myocardial stretch before contraction begins.


 - The Starling curve graphs the relationship between stretch and force.
    . The X-axis represents end-diastolic volume [ which determines sarcomere
     length]
    . The Y-axis represents the stroke volume and is an indicator of the
      force of contraction.
    . Frank - Starling law of the heart
      As additional blood enters the heart, the heart contracts more
      forcefully and ejects more blood from the heart.
      [ The heart pumps all the blood that returns to it.]


-Stroke volume and venous return
- venous return is the amount of blood that enters the heart from the venous
  circulation. Venus return is affected by three things:
    (a) contraction or compression of veins returning blood to the heart
        [skeletal muscle pump].
         - The skeletal muscle pump is simply skeletal muscle contractions
           that squeeze veins forcing them to push blood toward the heart.
         - During exercise of legs in particular, the SMP helps return blood
           to the heart.
         - During periods of sitting or motionless standing, the SMP does not
           aid venous return.
    (b) pressure changes in the abdomen and thorax during breathing.
        [respiratory pump]
         - The respiratory pump is created by movement of the thorax during
           inhalation.
         - The thoracic cavity expands which creates pressure that is below
           atmospheric. This pressure decreases pressure in the inferior vena
           cava as it passes through the thorax. In turn, this helps draw
           more blood into the vena cava from veins in the abdomen.
    (c) sympathetic innervation of veins.
        - constriction of veins by sympathetic activity.
        - When veins constrict, they squeeze more blood out of them and into
          the heart.


- Contractility is controlled by the nervous and endocrine systems
   - intropic agent is any chemical that affects contractility.
   - intropic effect is the influence of the intropic agent.
       (a) Inotropic effects are positive if the intropic agent increases the
           force of contraction. [example: catacholamines]
       (b) Inotropic effects are negative if the intropic agent decreases the
           force of contraction.
A muscle can remain at one length but show increased contractility because
contractility increases as the amount of calcium available for contraction
increases.
Increasing sarcomere length also makes the cardiac muscle more sensitive to
Ca2+, therefore linking contractility to muscle length.


- EDV and arterial blood pressure determine afterload.
 - afterload is the combined load of EDV and arterial resistance during
    ventricular contraction.


 - To maintain constant stroke volume when afterload increases, the ventricle
   has to increase its force of contraction, which then increases the muscles
   need for oxygen and ATP.


- ejection fraction is the percentage of EDV ejected with one contraction.
   [stroke volume/EDV]
Chapter Summary
(1) Cardiovascular anatomy review: the heart.
(a) The human cardiovascular system consists of a heart that pumps blood
    through a closed system of blood vessels.
(b) The primary function of the cardiovascular system is the transport of
    nutrients, water, gases, wastes, and chemical signals too and from all
    parts of the body.
(c) Blood vessels that carry blood away from the heart are arteries.
    blood vessels that return blood to the heart are veins.
    Valves in the heart and veins prevent the backflow of blood.
(d) The heart is divided in half by the septum, each half has an atrium and a
    ventricle.
(e) The pulmonary circulation goes from the right side of the heart to the
    lungs and back to the heart.
(f) The systemic circulation goes from the left side of the heart to the
    tissues and back to the heart.


(2) Pressure, volume, and flow resistance
(a) Blood flows down a pressure gradient from the highest pressure [in the
    aorta] to the lowest pressure [in the venae cava and the pulmonary
    veins]
(b) In a system in which fluid is flowing, pressure decreases over distance.
(c) The pressure created when ventricles contract is called the driving
    pressure.
(d) Resistance of a fluid flowing through a tube increases as the length of
    the tube and the viscosity of the liquid increase, and the radius of the
    tube decreases.
    Of these three factors, radius has the strongest influence on resistance.
(e) Fluid flow through a tube is proportional to the pressure gradient.
    A pressure gradient is not the same thing as the absolute pressure in the
    system.
(f) Flow rate is the volume of blood that passes one point in the system per
    unit time.
(g) Velocity of flow is the distance a volume of blood travels in a given
    period of time. At a constant flow rate, the velocity of flow through
    a small tube is faster than the velocity of flow through a larger tube.


(3) Cardiac muscle and the heart
(a) The heart is composed mostly cardiac muscle [or myocardium]
    Most cardiac muscle is a typical striated muscle.
(b) The signal for contraction originates in autorhythmic   cells in the
    heart. Autorhythmic   cells are noncontractile myocardium.
(c) Myocardial cells are linked to one another by intercalated disks that
    contain gap junctions. The gap junctions allow depolarization to spread
    quickly from cell to cell.
(d) In contractile cell excitation-contraction coupling, an action potential
    opens Ca2+ channels. Ca2+ entry into the cell triggers the release of
    additional Ca2+ from the sarcoplasmic reticulum through calcium-induced
    calcium release.
(e) The force of cardiac muscle contraction depends on how much Ca2+ enters
    the cell.
(f) As initial muscle fiver length increases, the force of contraction also
    increases.
(g) The action potentials of myocardial contractile cells have a rapid
    depolarization phase created by Na+ entering the cell. They also have a
    steep repolarization phase due to K+ leaving the cell. The action
    potential also has a plateau phase created by Ca2+ entering the cell.
(h) Autorhythmic   myocardial cells have an unstable membrane potential
    called a pacemaker potential. The pacemaker potential is due to If
    channels that allow net influx of positive charge.
(i) The steep depolarization phase of the autorhythmic   cell action
    potential is caused by the Ca2+ entering the cell. Repolarization phase
    is caused by K+ leaving the cell.
(j) Norepinephrine and epinephrine act on beta receptors to speed up the rate
    of the pacemaker depolarization and increase heart rate. Acetylcholine
    activates muscarinic receptors and slows down heart rate.


(4) The heart as a pump
(a) Action potentials originate at the sinoatrial node and spread rapidly
    from cell to cell in the heart. Action potentials are followed by a wave
    of contraction.
(b) Pathway of the electrical signal:
     SA node through the internodal pathway to the
     atrioventricular node then into the
     AV bundle  bundle branches  terminal Purkinje fibers
     Myocardial contractile cells.
(c) The SA node sets the pace of the heartbeat. If the SA node malfunctions
    other autorhythmic   cells in the AV node or ventricles will take control
    of heart rate.
(d) An electrocardiogram is a surface recording of the electrical activity
    of the heart.
     .P wave represents depolarization
     . QRS complex represents ventricular depolarization
     . T wave represents ventricular repolarization.
(e) An ECG provides information on heart rate and rhythm, conduction
    velocity, and the condition of cardiac tissues.


(5) The cardiac cycle
(a) One cardiac cycle includes one cycle of contraction and relaxation.
    Systole is the contraction phase.
    Diastole is the relaxation phase.
(b) Most blood enters the ventricles while the atria are relaxed. Only 20%
    of ventricular filling at rest is due to atrial contraction.
(c) The AV valves prevent backflow of blood into the atria.
    Vibrations of closing AV valves create the first heart sound.
(d) During isovolumic ventricular contraction, the ventricular blood volume
    does not change, but pressure increases. When ventricular pressure
    exceeds the atrial pressure, the semilunar valves open and blood is
    ejected into the arteries.
(e) When the ventricles relax and ventricular pressure falls, the
    semilunar valves close, which creates the second heart sound.
(f) The amount of blood pumped by one ventricle during one contraction
    relaxation cycle is the stroke volume.


(6) Cardiac output
(a) Cardiac output is the volume of blood pumped per ventricle per unit
    time. Cardiac output can be calculated by multiplying the heart rate by
    the stroke volume.
(b) Homeostatic changes in cardiac output are accomplished by varying
   heart rate, stroke volume, or both.
(c) Parasympathetic activity slows heart rate
    Sympathetic activity increases heart rate.
(d) Frank-Starling law of the heart states that an increase in
    end-diastolic-volume results in a greater stroke volume.
(e) Epinephrine and norepinephrine increase the force of myocardial
    contraction when they bind to beta-agrenergic receptors. They also
    shorten the duration of the cardiac contraction.
(f) End-diastolic volume and preload are determined by venous return.
(g) Venous return is affected by skeletal muscle contractions, the
    respiratory pump, and constriction of veins by sympathetic
    activity.
(h) Contractility of the heart is enhanced by catecholamines and certain
    drugs. Chemicals that alter contractility are called inotropic agents and
    their effects are called inotropic effects.
(i) Afterload is the load placed on the ventricle as it contracts.
    Afterload reflects the preload and the effort required to push the blood
    out into the arterial system. Mean arterial pressure is a clinical
    indicator of afterload.
(j) Ejection fraction is the percent if EDV ejected with one contraction.
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