I.  Review of anatomy of heart
 A.  Chambers
  Layers of tissue
  Myocardium--syncytium of intercalated disks, functional     significance
  chambers each form independent syncytium
 B.  Valves
  One way doors
  Opening and closing governed by pressure
 C.  Flow of blood through chambers, lungs, valves

II.  Electrical Activity of the Heart
 A. Types of cardiac muscle fibers
  1.  Self-excitable cells
   depolarization of self-excitable cells is the electrical      conducting system of the heart
  2.  Contractile cells
   these cells contract after electrical stimulus (arriving     from self-excitable cells) bring the contractile      cells to threshold
 B.  Self-excitable cells (aka pacemaker cells and why I think    that’s a misnomer)
  1.  Characteristics of a self-excitable cell
   -depolarizes spontaneously
    -doesn’t REQUIRE nervous input for        depolarization but can  be affected by       the nervous system, hormones, drugs,       etc.
  2.  The self-excitable cells of the heart
   a.  Sinoatrial node
   b.  Atrioventricular node
   c.  Bundle of His
   d.  Purkinje fibers
  3.  Conduction of electrical activity in the heart
   a.  SA node is the pacemaker
   b.  Interatrial pathway
   c.  Internodal pathway
   d.  Nodal Delay
   e.  Bundles of His
   f.  Purkinje fibers
   g.  Gap jxns
  4.  Critical characteristics of electrical spread
   a.  coordinate contraction of each heart chamber
    -fibrillation
   b.  left and right side contract at same time to pump      blood into lungs & systemic circulation (avoids      pooling)
   c.  AV nodal delay so that atrial contraction complete     before ventricles begin contracting
  5.  Mechanism of self-excitability.
   a.  Drift to threshold
    i.e. RMP not constant
    -origin of drift to threshold somewhat unclear
    -spontaneous decrease in permeability to K,      therefore less K leaks out and inside of cell      becomes less negative, drifting to potential
   b. Rapid rise
    At threshold, voltage-gated calcium channels       open
    Ca influx depolarizes cell
   c.  Falling phase
    Opening of voltage-gated K channels
    K efflux
    Repolarization
   d.  Summary picture
 
 
 
 
 
 
 
 

 C.  Contractile Cells

  1.  Characteristics of contractile cells
   a.  Striated
   b.  Thick and thin filaments arranged in regular array     as in skeletal  muscle
   c.  Contraction initiated by increased cytosolic       calcium (just as in skeletal muscle, with Ca      binding to troponin)
  2.  Action potentials in cardiac contractile cells
   a.  Constant RMP
   b.  Excitation of c.c. cell through electrical impulse      originating at SA  node
    1.  Opening of voltage gated Na channels
    2.  Plateau phase
     -closing of Na channels
     -opening of slow Ca channels, so long        slow influx of Ca
    3.  Repolarization due to:
     -closing of Ca channels
     -opening K channels so rapid efflux of K
  3.  Important facets of the plateau phase
   a.  calcium influx due to opening of calcium channels     not only depolarizes muscle cell, allowing for      electrical release of calcium from organelles      within cell, but also can be used to bind       troponin

Q:  What would measuring cardiac form of troponin in blood be diagnostic for?

   b.  long refractory period during action potential      means that it’s difficult to initiate another       muscle contraction until the heart muscle has      contracted and relaxed (allowing filling)

 D.  Pathology of electrical activity of heart

  1.  Ectopic pacemakers

  2.  Fibrillation

  3.  Tachycardia/Bradycardia

  4.  Heart Block
 

II.  The heart as a pump
 A.  Pressure volume relationships within the heart
  1.  Increased volume in closed space leads to increased     pressure
  2.  Muscle contraction leads to increased pressure
  3.  Pressure differences across valves and       opening/closing of valves
 B.  Basic events
  1.  Systole
   a.  Contraction
   b. occurs following depolarization of muscle
   c.  necessary for pumping blood from chamber to      chamber and for ejection into peripheral       circulation
  2.  Diastole
   a.  Relaxation
   b.  occurs following repolarization of muscle
   c.  necessary for filling the heart with blood
 C.  The cardiac cycle
  1.  Passive filling of atria and ventricles during diastole
   a.  Blood enters the atria passively
   b. AV valves are open
   c.  passive filling of ventricles (rapid filling due to      blood pooled in atria while AV valve closed      during ventricular systole)
  2.  Active pumping of blood from atria to ventricles       following atrial contraction
  3.  Isovolumetric contraction of ventricles
   a.  All valves shut (AV valves and semilunar valves)
   b.  Increased pressure in ventricles
  4.  Ventricular ejection
   a.  Semilunar valves open when pressure in      ventricle exceeds pressure in pulmonary artery or      aorta
  5.  Isvolumetric relaxation of ventricles
   a.  No change in volume of blood in ventricles       because all valves are closed again
   b.  Blood pools in atria

 D.  The Wiggers Diagram (fig. 9-5) (left side of heart, but right is    similar with lower values)
  1.  ECG
   P=atrial depolarization
   QRS=ventricular depolarization
   T= ventricular repolarization
  2.  Atrial pressure
  3.  Ventricular volume
  4.  Ventricular pressure
  5.  Aortic pressure
  6.  ECG
  7.  Heart sounds (phonogram)  valves closing yield 1st     and second heart sounds

  How to read and interpret the graph
 E.  Heart Murmurs
  Normal blood flow is quiet while turbulent flow is loud.     Fluid passing through narrow area makes noise.
  1.  Stenotic valve
   -fibrous, stiff and can’t open completely
   -you will hear a whistle when the valve is supposed      to open
   -when are semilunar valves open? (during systole)
   -when are AV valves open (during diastole)
 

  2.  Insufficient valves (leaky)
   -valve is weak and seal is poor
   -blood regurgitates
   -swishing sound heard when valves should be     closed
   -when are semilunar valves closed?  AV valves?

III.  Regulation of Heart Pumping
 A.  Cardiac Output
  1.  Definitions
   a.  C.O. volume pumped per minute
   b.  SV
    EDV-ESV
    Volume after ventricles are filled-volume       remaining after ventricular ejection
  2.  C.O. = H.R. x S.V.
  3.  Cardiac reserve
   -The difference in cardiac output at rest (5L/min)      and at C.O. max
   -in severe exercise may increase CO by 4-7 times

 B.  Intrinsic Control
  1.  Frank-Starling Law of the Heart
   -stretching muscles increases force of contraction
   -increased filling of heart increases cardiac output
    e.g. increased venous return or increased      EDV leads to increased SV
   -Heart pumps out the volume of blood returned to it
 C.  Extrinsic Innervation of the Heart
  1. Cardioacceleratory center
   a. in medulla oblongata
   b. sympathetic nerves (what do they release?)
    -release of epinephrine from the adrenal can       act on b-adrenergic receptors in the       heart
   c. innervates SA, AV node
    -acts to increase SA node discharge
    -decrease AV nodal delay
    -mechanism probably by increasing       permeability to Na and Ca
    -increases heart rate
   d. increases contractility of muscle
    -mechanism may be by increasing cytosolic       Ca
   e.  Summary
   Sympathetic increases C.O. by:
    *decreasing ESV (increased contractility leads      to less volume remaining in ventricle)
    *increasing HR
    *increasing EDV (increased venous return)       due to vasoconstriction
  2.  Cardioinhibitory centers
   a.  also located in medulla oblongata
   b.  vagus nerve (parasympathetic nerve)
   c.  releases what neurotransmitter to act on what      receptor (Ach on muscarinic receptors)
   d.  innervates SA and AV nodes to inhibit HR and      slow conduction through AV node
   e.  minor effects on contractility
   f.  At rest, the PS system predominates
    Q:  What will happen if you cut the vagus nerve     or drip Ach on heart?

IV.  Pathology of the Pump
 A.  Coronary atherosclerosis
  1.  Decreased blood and oxygen delivery to cardiac cells results in ineffective contraction
 B.  Persistent high blood pressure
  1.more difficult to eject blood into aorta
  2. hypertrophy of left side of heart
  3. eventual weakening of muscle
 C.  Myocardial infarction
  1.   Death of cardiac muscle
   -occlusion of coronary blood vessels is cause
  2.  noncontractile tissue decreases pumping efficiency
 D.  Congestive heart failure
  1.  Pulmonary congestion as blood backs up when      inadequate ejection from left side occurs
  2.  Pulmonary edema
  3.  Inadequate C.O. and gas exchange in lungs
 E.  Compensation mechanisms
  1.  Sympathetic stimulation
  2.  Kidneys
   a.  retain more water to increase EDV and thus     SV (F-S curve)
   b.  double-edged sword because increased water      retention leads to increased afterload which      futher weakens heart
 F.  Treatment
  1.  Digitalis
   increases cytosolic calcium to increase contractility
   decreased HR to increase filling time and thus       contractility
  2.  Epinephrine
  3.  Diuretics

V.  Fetal/neonatal cardiovascular physiology (Fig. 83-4)
 A.  Unique organization of fetal circulation
  1.  Why does fetal circulation differ?
   a.  Lungs are non-functional and not expanded
    -high resistance to pulmonary circulation
   b.  Liver is only partially functional
   c.  Placental circulation requires that the fetal heart      pump blood through placenta
  2.  Differences
   a.  Presence of foramen ovale
    -highly oxygenated blood from placenta        enters right atrium and is shunted to left       atrium, bypassing lungs
   b.  Ductus venosus
    -venous blood from placenta bypasses liver
   c.  Ductus arteriosus
    -shunt between the pulmonary trunk and the       aorta
    -small portion of blood leaving right ventricule       is pumped into lungs but most enters       ductus arteriosus to be sent to placenta       for oxygenation

 B.  Changes in fetal circulation at birth
  1.  Closure of foramen ovale
   a.  Higher systemic vascular resistance (loss of low     resistance placental circulation)
   b.  Higher pressure in left atrium pushes closed the     valve on foramen ovale
   c.  Valve becomes adherent to atrial septum in most     people within a few months
  2.  Closure of the ductus venosus
   a.  Muscle contraction
  3.  Closure of ductus arteriosus
   a.  Low pulmonary resistance as lungs expand
   b.  High aortic pressure
   c.  Little circulation through ductus arteriosus
   d.  Constriction of smooth muscle and eventual     occlusion by growth of connective tissue into lumen
   e.  Patent ductus arteriosus
    ---remains open
    -causes recirculation of left ventricular blood       through the lungs, with several passes       for every pass through systemic        circulation
    -recirculation leads to increased volume       output of left ventricle
    -less cardiac reserve so strenuous exercise      leads to weakness and fainting
    -pulmonary congestion