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Cardiac Muscle I

Cardiac Muscle I. Essential Features of Vertebrate Cardiac Muscle. Striated Cells connected by gap junctions Dually innervated by ANS Spontaneously active, either normally or in disease states, depending on the cell type. In mammals : highly dependent on oxidative metabolism.

katalin-molnar
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Cardiac Muscle I

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  1. Cardiac Muscle I

  2. Essential Features of Vertebrate Cardiac Muscle • Striated • Cells connected by gap junctions • Dually innervated by ANS • Spontaneously active, either normally or in disease states, depending on the cell type. • In mammals: highly dependent on oxidative metabolism

  3. Differentiation of Functional Cell Types in the Heart • Nodal fibers- spontaneously active pacemakers that can initiate heartbeat • Conducting fibers - rapidly carry excitation from one part of the heart to another • Myocardial fibers - compose most of the mass of the heart and provide essentially all of the force.

  4. Nodal and conducting fibers in the heart

  5. Sequence of electromechanical events in a heartbeat • Spontaneous AP in SA nodal pacemakers • Excitation spreads throughout atria, followed by atrial contraction • Excitation reaches AV node, enters bundle of His, is conducted into both ventricles by branch bundles, and is rapidly spread throughout the ventricular myocardium by Purkinjie fibers - followed by ventricular contraction or systole.

  6. Agenda of topics to consider • Nature of pacemaker action potentials • Control of heart rate by the ANS • Nature of myocardial action potentials • Relationship between myocardial action potentials and the electrocardiogram • Myocardial excitation-contraction coupling • Control of myocardial contractile force by stretch and by autonomic inputs

  7. Action potentials recorded from the ventricular myocardium, SA node and atrial myocardium. The total time in each window is about 300 msec for the myocardial cells and about 150 msec for the SA nodal cell.

  8. Pacemaker potentials • Nodal cells (pacemakers) do not have stable resting potentials. • Instead, the cells undergo a spontaneous, slow depolarization (prepotential) until threshold is reached. • The upstroke of the AP is slow compared to nerve and skeletal muscle. • Each action potential leads to a temporary afterhyperpolarization that leads into the next prepotential.

  9. If inward K+ T Ca++ L Ca++

  10. The rate of pacemaker potentials is modulated by the autonomic NS • In the absence of any autonomic input, the natural rate of pacemaker potentials is about 100/min in human heart. • Cholinergic input slows the heart rate by slowing depolarization during the prepotential; adrenergic input increases the heart rate by increasing the rate of depolarization.

  11. This slide shows the effects of isoproterenol (a beta agonist; A), stimulation of the vagus nerve (B), and two concentrations of Ach. Before and after traces are overlain; c indicates control beats and * experimental beats.

  12. How beta1 receptors increase heart rate • Second messenger: cAMP (slow), but directly by Gs (rapid) • Channel effects: • 1. shift activation of L channels to more negative voltages, causing threshold to be reached sooner; increase current carried by L channels. • 2. Increase If, causing hypolarization at beginning of prepotential to be smaller.

  13. How muscarinic receptors slow the heart • Second messengers: Gi-mediated inhibition of adenylyl cyclase (slow); but direct effect of Gi on K+ channels (rapid). • Channel effects: • 1. Open Ach-sensitive K+ channels • 2. Shift L channel activation to more positive voltage values and decrease channel conductance. • 3. Decrease If, causing a greater hyperpolarization at the beginning of the prepotential.

  14. Key features of the myocardial action potential • Rapid upstroke • LONG plateau • Potential relatively stable during the interbeat interval, except in disease.

  15. Channels involved in the myocardial AP “fast” Na+ channels L Ca++ channels K+ channels (several types)

  16. The electrocardiogram is an extracellular recording of the myocardial AP • Voltage is measured at several spots on the body surface - because body fluid is a conductor of electricity, these spots could be thought of as wires connected directly to the heart surface. • A voltage difference will exist only when some parts of the heart are depolarized while others are not. During the interbeat interval, OR when the ventricle is all depolarized, the EKG trace will return to baseline.

  17. If we measure the voltage difference between the right arm and left leg over a heart cycle, we will watch excitation start in the atria, spread through the ventricles, and end with ventricular repolarization

  18. Relationship between atrial and ventricular AP s and EKG waves Atrial Ventricular

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