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Cardiac Physiology

Cardiac Physiology. The heart: chambers, the valves Cardiac muscle cells Some cardiac muscle cells are autorhythmic Arrangement of cardiac muscle cells Excitation-contraction coupling. Atrioventricular (AV) Valves. guard the passageway between the atria and the ventricles

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Cardiac Physiology

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  1. Cardiac Physiology • The heart: chambers, the valves • Cardiac muscle cells • Some cardiac muscle cells are autorhythmic • Arrangement of cardiac muscle cells • Excitation-contraction coupling

  2. Atrioventricular (AV) Valves • guard the passageway between the atria and the ventricles • Tricuspid valve between right atrium and right ventricle • Bicuspid (mitral) valve between left atrium and left ventricle

  3. Semilunar valves • Between ventricles and arteries • Pulmonary valve between right ventricle and pulmonary artery • Aortic valve between left ventricle and aorta

  4. All myocardial cells • Gap junctions at intercalated discs, waves of depolarization spread from one cell to another

  5. Autorhythmic myocardial cells • (pacemakers) are small myocardial cells with few contractile fibers • Spontaneously generate action potentials • Enables the heart to contract without any outside signal • The heart is myogenic: signal for contraction originates from heart muscle itself

  6. Most myocardial cells • Remaining myocardial cells are striated • Have sarcomeres • Much smaller than skeletal muscle fibers • Connected by gap junctions at intercalated discs • Lots of mitochondria • Lots of blood flow to myocardial cells

  7. More facts about myocardial cells • Large branching t-tubules • Sparse sarcoplasmic reticulum • Source of Ca++ is largely extracellular

  8. Excitation-contraction coupling • Depolarization cell membrane voltage gated Ca++ channels open •  Ca++ enters cell •  calcium-induced calcium release: Ca++ released from SR •  Ca++ binds to troponin contraction

  9. Myocardial cell relaxation • Ca++ dissociates from troponin •  Ca++ returns to SR by Ca++ ATPase •  Ca++ also transported from cell by Na+-Ca++ indirect active transport protein: Ca++ is exchanged for Na+, which moves in along its electrochemical gradientNa+ removed by active transport

  10. Regulation of cardiac muscle contraction • Graded contractions • Effect of cardiac muscle stretching • Channel activity during action potentials • In myocardial contractile cells • In autorhythmic pacemakers

  11. Graded contraction • The amount of force varies with the number of cross-bridges formed • Low Ca++ few cross-bridges • High Ca++ more cross-bridges

  12. The effect of epinephrine and norepinephrine of contraction • NE and E bind to beta 1 receptors on contractile myocardial cells • The beta 1 receptor is coupled to a G protein • Cyclic AMP is formed

  13. The effect of epinephrine and norepinephrine of contraction • cyclic AMP is formed  • 1. Voltage gated Ca++ channels are phosphorylated stay open longer  more intracellular Ca++ stronger contractions • 2. A regulatory protein, phospholamban, is phosphorylated increased activity on SR Ca++ ATPase contractions shorten duration

  14. Effect of phospholamban on Ca++ release • NE and E activity • increase phospholamban activity • increase Ca++ ATPase activity on SR • more Ca++ is sequestered into the SR • more Ca++ is available for Ca++ release during stimulation • stronger force of contraction

  15. Effect of NE and E on contraction • Stronger, more frequent contractions

  16. When myocardial cells elongate • The amount of Ca++ entering the myocardial cells may increase  the force of contraction increases

  17. Myocardial contractile cell action potentials • Resting potential is stable -90 mV • Wave of depolarization through gap junctions • Voltage gated Na+ channels open • Voltage gated K+ channels open • Slow voltage gated Ca++ channels open and K+ channels close • Ca++ channels close and K+ channels open

  18. Long action potential • Myocardial cell refractory period and contraction end simultaneously

  19. Action potentials in myocardial autorhythmic cells • The channels: • If channels allow passage of Na+ and K+ • Ca++ channels

  20. Action potentials in myocardial autorhythmic cells • Unstable resting membrane potential • Pacemaker potential • At a membrane potential of -60 mV Na+ enters through the If channels •  mb depolarizes •  Ca++ channels open •  Ca++ channels close •  K+ leaves

  21. Modulation of autorhythmic cells • NE (sympathetic) and E (adrenal hormone) • Autorhythmic cells have beta1 receptors • Cyclic AMP levels increase • Properties of If and Ca++ channels altered • More rapid Na+ and Ca++ entry • Rapid action potential • Rapid contractions

  22. Modulation of autorhythmic cells • Parasympathetic, acetyl choline • Muscarinic receptors • K+ channels open mb hyperpolarizes cell less excitable • Ca++ channel less likely to open slower depolarization  cell is less excitable

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