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Cardiovascular Physiology 

  • Cardiac muscle physiology overview:

    • Three major types of cardiac muscle

      1.  Atrial muscle-similar to skeletal muscle but with a longer contraction duration

      2.  Ventricular muscle-similar to skeletal muscle but with a longer contraction duration

      3.  Specialized muscle of the cardiac conducting system-few contractile fibers, hence limited contractility: important because of their central role in cardiac electrical excitation

    • Histological aspects

        • Cardiac muscle striated-similar appearance to skeletal muscle

        • Cardiac muscle cross-section (400X) (di Fiore's Atlas of Histology with Functional Correlations, , William L. Todt, Concordia College)

        •  Myofibrils containing (a) actin (b)  myosin filaments (extremely similar to those found in skeletal muscle)

        • Myofibril filaments interdigitate in a manner very much like that seen in skeletal muscle

       

    • Other anatomical aspects:

      •  Individual cardiac cells are separated from one another by "intercalated discs"

      •  Cardiac muscle fibers are composed those numerous individual cells connected in series to each other {intercalated discs do not interfere with electrical propagation (action potential propagation) through myocardial structures

      •  Because of this extensive interconnectivity without the electrical interruption, action potentials are typically propagated smoothly and progressively throughout the myocardium

      •  This "latticework" of cells is called  a syncytium, which describes cardiac muscle 

      •  The heart is composed of two syncytiums-- the atrial syncytium which includes the two atrial walls and the ventricular syncytium composed of the two ventricular walls

    • Barriers to conduction

      • Fibrous tissue between the atria and ventricles are characterized by high electrical resistance such that myocardial action potential propagated from the atrial syncytium to the ventricular syncytium through the specialized conduction system called the AV node (atrioventricular (AV) bundle)

    • Important consequence of 2 syncytium structures: the separate structures allow the atria to contract in time slightly before the ventricles -- a condition central to the cardiac pumping effectiveness

  • Myocardial Action Potential

    • Resting membrane potential

      • -85 to -90 mV for normal cardiac muscle

      • -90 to -100 mV for specialized conducting fibers, e.g. bundle of His,  AV nodal fibers

    • Action potential

      • Magnitude for ventricular muscle = about 105 mV (i.e., going from about -85 mV to + 20 mV): this abrupt change in membrane potential corresponds to the "spike"

      • Depolarization duration = about 0.2 seconds for atrial muscle & about 0.3 seconds for ventricular muscle

      • Plateau phase: extends the duration of the action potential significantly (3-15 times) relative to the action potential duration of skeletal muscle

    • Ions and the myocardial action potential:

      •  "Fast" response component -- due to activation of fast sodium channels:

        • At normal resting membrane potentials, activation of sodium channels involves large number of channels opening in a synchronous manner

        • The large number of rapidly and synchronously opening channels results in a significant inward sodium current which is the basis for typically rapid conduction & action potential propagation through the heart

      • "Slow" response component-due to activation of slow calcium channels

        • Remain open longer than sodium channels

        • Responsible for the plateau phase of the action potential

        • Ca2+ ions entering the cell facilitates also leading muscle  contractile process

      •  Recovery of the resting membrane potential

        • Following Na+ and Ca2+ ion channel activation and then inactivation, membrane K+  permeability increases

        • K+ efflux results in repolarization.

         

    • Comparison between the Time-Course of the Action Potential and Contractile Force Development

     

  • Conduction Velocity

    •   Atrial/ventricular muscle fibers: 0.3-0.5 meters per second

    •  Specialized fibers for action potential propagation through the heart (e.g. Purkinje fibers): 0.02-4 m per second

  • Refractory Period

    •  Definition: amount of time following an action potential during which the normal cardiac impulse cannot re-excite the previously excited tissue:  this is the absolute refractory period

      • Duration -- normal absolute refractory period = 0.25-0.3 seconds

    •  Relative refractory period:

      • Cardiac muscle may be excited, but with greater difficulty than normal.  

      • Duration: approximately 0.05 seconds (adds somewhat to the absolute refractory period)

    • Atrial refractory period (absolute refractory = 0.15 seconds; relative refractory = 0.03 seconds) -- shorter than ventricular refractory period. As a consequence, atrial contraction rates may be significantly higher than ventricular contraction rates

  • Relationships between membrane depolarization and muscle contraction

    • Term: excitation contraction coupling

    • Sequence of events:

      1.  Action potential spread

        • over the surface

        • to the interior of the cardiac muscle fiber along transverse (T) tubules

      2.  T tubule action potential causes Ca2+ ion release from the muscle sarcoplasmic reticulum into the muscle sarcoplasmic {calcium ion are also released from the T tubules themselves, providing extra Ca2+ ions the lesson adding to the strength of cardiac muscle contraction. [this case is in contrast to skeletal muscle in which Ca2+ ions are released essentially only from the sarcoplasmic reticulum; skeletal muscle sarcoplasmic reticulum is better developed than the myocardial counterpart which stores less calcium]

      3.  Ca2+ ions diffuse into the myofibrils where upon binding to troponinC actin-myosin interaction and sliding are initiated.

    • Myocardial contraction strength calcium dependencies:

      • Significantly influenced by extracellular calcium concentration [Ca2+ ] because ends of the T tubules open extracellularly, allowing T tubule [Ca2+ ] equilibration with extracellular [Ca2+ ] .

        • This relationship between extracellular [Ca2+ ] and myocardial contractility explains why hypocalcemia or calcium channel antagonists would be expected to depress myocardial contractility.

    •  

      Different Forms of Cardiac Action Potential, Depending on Anatomical Location and Cell Type

      • Slightly modified from: Crawford, M. H. and DiMarco, J. P, Cardiology, Mosby, St. Louis, MO. 2001

 

  • Electrophysiology: Pacemaker and Cardiac Cells 
    American Association of Critical-Care Nurses (AACN)
  • Left to right: pacemaker cell, atrial muscle cell, ventricular muscle cell

    • Figure by: Barbara McLean, MN, RN, CCRN, CRNP
       

 

Cardiac Conduction System: Review

 

Automaticity

 

 
 
 
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  • Primary Reference: Guyton, AC,  "Heart Muscle; The Heart as a Pump, Chapter 9, in Textbook of Medical Physiology 9th Edition, W. B. Saunders Company, Philadelphia, pp. 107-119, 1996.
  • Primary Reference:  Ross, AF, Gomez, MN. and Tinker, JH Anesthesia for Adult Cardiac Procedures in  Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds)  Mosby, St. Louis, Mo., pp. 1659-1698, 1998.
  • Primary Reference: Blanck, Thomas J.J. and Lee, David L, Cardiac Physiology, in Anesthesia, 5th edition,vol 1, (Miller, R.D, editor; consulting editors, Cucchiara, RF, Miller, Jr.,ED, Reves, JG, Roizen, MF and Savarese, JJ) Churchill Livingston, a Division of Harcourt Brace & Company, Philadelphia, pp. 619-646, 2000.
  • Primary Reference:  Berne, R.M and Levy, M. N. Cardiovascular Physiology,8th Edition, Mosby, St. Louis, Mo. 2001
  • Primary Reference: Crawford, M. H. and DiMarco, J. P, Cardiology, Mosby, St. Louis, MO. 2001
  • Shanewise, JS and Hug, Jr., CC, Anesthesia for Adult Cardiac Surgery, in Anesthesia, 5th edition,vol 2, (Miller, R.D, editor; consulting editors, Cucchiara, RF, Miller, Jr.,ED, Reves, JG, Roizen, MF and Savarese, JJ) Churchill Livingston, a Division of Harcourt Brace & Company, Philadelphia, pp. 1753-1799, 2000.
  • Wray Roth, DL, Rothstein, P and Thomas, SJ Anesthesia for Cardiac Surgery, in Clinical Anesthesia, third edition  (Barash, PG, Cullen, BF, Stoelting, R.K, eds), Lippincott-Raven Publishers, Philadelphia, pp. 835-865, 1997
  • Primary Reference: Garcia, T.B and Holtz, H.E., 12-Lead ECG:  The Art of Interpretation, Jones and Bartlett Publishers, Boston, 2001