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Cardiac Muscle

Cardiac Muscle. Figure 1.02. The cardiac cycle in terms of time. Figure 1.02B. Left heart pressures during one cardiac cycle. Figure 1.02C. Ventricular blood volume during one cardiac cycle. Figure 1.02D. Aortic blood flow during one complete cardiac cycle.

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Cardiac Muscle

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  1. Cardiac Muscle

  2. Figure 1.02. The cardiac cycle in terms of time

  3. Figure 1.02B. Left heart pressures during one cardiac cycle

  4. Figure 1.02C. Ventricular blood volume during one cardiac cycle

  5. Figure 1.02D. Aortic blood flow during one complete cardiac cycle

  6. Figure 1.02E. ECG and heart sounds during one cardiac cycle

  7. Figure 1.02F. Right heart pressures during one cardiac cycle

  8. Figure 1.05. Normal blood pressure and oxygen saturation values

  9. Length-tension curves (diagrams) for skeletal and cardiac muscle

  10. Figure 12M0. The effect of norepinephrine in augmenting tension and rate of tension development (Inotropicity) produced during isometric muscle twitches

  11. Figure 14.Bowditch effect (ie., Treppe, Staircase, force frequency relationship)

  12. Refractory Period: • Long, compared to skeletal muscle • Prevents tetanus, guarantees a period of filling • Prevents ineffective tachycardia • Prevents re-entry ("circus" movement)

  13. Two Kinds of Myocardial Cells: • Pacemaker - exhibit automaticity (rising phase 4 prepotential) • primary - SA nodal • reserve - SA nodal, purkinje, AV nodal • Follower - no automaticity • (stable phase 4 potential; atrium, ventricle)

  14. Figure 3. The various ion pumps of the cell.

  15. Figure 2M0. The three slow Ca++ channel states: resting, active, inactive."d" and "f" are upper and lower gates in the channel.

  16. Ion Channels: Fast - initial rapid inward Na+ current. - secondary outward K+ movement repolarization Slow* - Ca++ moves inward, responsible for maintained depolarization of the "plateau phase" (Phase 2) • * An increase in contraction frequency increases Ca++ movement inward, giving the "staircase" phenomenon (Treppe, Bowditch) in cardiac muscle.

  17. Figure 4M0. The fast sodium and slow calcium channels. The fast channel is in its "resting" mode;the slow channel is in its depolarization mode, ie. active state (Ca++ ions moving through). The black dot indicates Nifedipine attachment site.TTX = Tetrodotoxin, Nifedipine = a medically-used Ca++ channel blocker."m" and "h" are upper and lower gates in the Na+ channel."d" and "f" are upper and lower gates in the Ca++ channel.

  18. Figure 5M0. Changes in transmembrane potential before and during depolarization in various types of myocardial cells.Not all the depolarization / repolarizations look like that in Figure 1.

  19. Mechanisms for Changing Pacemaker Cell Automaticity: • Hyperpolarize/hypopolarize overdrive suppression • Alteration of slope (rate of rise) of pre-potential (diastolic potential) • Alteration of threshold; e.g. epinephrine increases gCa++ (hypopolarizes), acetylcholine increases gK+ (hyperpolarizes)

  20. Factors Determining Action Potential Conduction Velocity: • Amplitude & rate of change of action potential - increasing velocity, decreasing time • - if large, more likely to depolarize adjacent cells • Anatomy of conducting cells - increased diameter, increases conduction velocity • - number of interconnections • - longer nexus junctions (Purkinje cells) • "Cable Properties" of the conducting system

  21. Factors Affecting Conduction Through the AV Junction: • Speeds - • Catecholamines * • Atropine - blocks Acetylcholine • Quinidine - inhibits vagal effects • Slows Acetylcholine * * • Digitalis - central vagal (parasympathetic) stimulation • Inhibitors of acetylcholine esterase, Ca++ antagonists (e.g. verapamil) • An increased number of impulses arriving at AV junction increases refractoriness

  22. Various Conditions of Muscle Contraction: • Isotonic • Unloaded • Preloaded • Afterloaded (to less than isometric) • Isometric

  23. Comparing isotonic and isometric muscle contractions. • + indicates it occurs; - does not occur

  24. Figure 6M0. Isometric and isotonic skeletal muscle twitches following a single action potential

  25. Figure 9M0. Isometric twitch tension as it is influenced by preload (ie. initial length, Frank-Starling mechanism)

  26. Figure 10M0. Velocity of muscle shortening and power output as each is influenced by increasing afterload

  27. Figure 8M0. Velocity of shortening (isotonic contraction) as it is altered by afterload and preload

  28. Effects of Increased Preload on Velocity of Shortening, etc: • Increased velocity of shortening (isotonic) at any given afterload • Unaltered Vmax at zero afterload • Increased muscle length • Increased tension development (isometric)

  29. Effects of Afterload on Velocity of Shortening: • Maximum at no load • Zero at maximum load (isometric) • Intermediate with some, not maximum load

  30. Effects of Increased Inotropicity on Velocity of Shortening, etc.: • Increased velocity of shortening (isotonic) at any given afterload • Increased Vmax at zero afterload • Same muscle length • Increased tension development (isometric), and increased rate of contraction and relaxation

  31. Figure 13M0. Velocity of muscle shortening and the influence of a catecholamine such as norepinephrine (Inotropicity) in modifying the relationship

  32. Figure 7M0. Mechanisms for altering isometric tension in cardiac muscle vs skeletal muscle

  33. Factors Affecting Heart Rate: • Leading to an INCREASE: • decreased activity of baroreceptors in the arteries, LV, and pulm. circ. (1) • inspiration (2) • excitement, anger, most painful stimuli (1) • hypoxia (1?) • exercise (1) • norepinephrine (1) , epinephrine • thyroid hormones • fever • Bainbridge reflexLeading to a DECREASE: • increased activity of baroreceptors in the arteries, LV, and pulm. circ. (2) • expiration(1) • fear, grief (2) • stimulation of pain fibers in trigeminal nerve • increased intracranial pressure (Cushing Reflex) (1)

  34. Actions of Vagal Parasympathetic Neurons to the Heart (through release of acetylcholine) • ...... Site ................................ Action .......................................... Affecting ...... • sino-atrial node ................... decreases heart rate ........... chronotropicity • atrio-ventricular node ............ slowed AV conduction ..... chronotropicity • atrio-ventricular node .. delayed conduction / increased refractoriness ……………………………………………………………..chronotropicity • Note: There are few/no parasympathetic nerve endings on the ventricular myocardium, so while acetylcholine is a potential negative inotrope for the ventricles, it is not released there.

  35. Figure 2.01. Schematic of vagal escape. Acetylcholine release from parasympathetic ends on the SA nodeand AV node & Junctional tissue increases refractoriness and depresses conduction velocity.Intense stimulation will stop ventricular depolarization, ie. contraction. Reserve pacemakers come into play.

  36. Control of Cardiac Performance: STROKE VOLUME: • Extrinsic: • Release of the following substances from the sympathetic and parasympathetic sympathetic branches of the autonomic nervous system, affect inotropicity: • norepinephrine (+) - neural • acetylcholine (-) - neural* • epinephrine (+) - blood borne These actions are mediated through cardiopulmonary receptors, such as the carotid sinus (aortic) baroreceptors, carotid (aortic) body chemoreceptors, central chemo-receptors, venae cavae/atrial volume receptors (Bainbridge), and the ventricular volume receptors. • Attention: Inotropicity (ie. contractility) and strength of contraction are not synonomous. Increased / decreased strength of contraction can be achieved by changing preload(ie. Frank-Starling) with no change in inotropicity. Inotropicity reflects the biochemical state within the muscle (eg. Ca<SUP++< sup>, ATP), not simply the positioning of the thick and thin • myofilaments as determined by stretch. Intrinsic: • Frank-Starling - through preload (heterometric autoregulation) • afterload - through increased / decreased arterial blood pressure acting on aortic valve. • Anrep effect - laboratory curiousity? • Bowditch effect } (homeometric autoregulation) (Treppe, Staircase) • environment - ischemia, O2, CO2 • cardiac hypertrophy - longterm effect * In actual fact, there are few parasympathetic fibers in the ventricular myocardium, so ACH has little practical effect physiologically on ventricular inotropicity (contractility).

  37. Figure 2.02. Frank-Starling (or ventricular function) curve. See cardiac muscle length-tension curve.The black curve defines a single inotropic state.

  38. Major Factors Determining Myocardial Stretch: • Total blood volume • Body position relative to the earth and gravity pull • Intrathoracic pressure • Intrapericardial pressure • Venous tone • Pumping action of the skeletal muscle • Atrial contribution to ventricular filling

  39. Figure 2.03. Some factors contributing to afterload. What are shown here are the effects of increased vascular resistance and vascular compliance. Another major factor not shown is heart dimension, ie. a dilated heart sustains greater afterload at the same arterial or ventricular pressure than a smaller heart (a larger heart has larger radii of curvature and through the Law of Laplace is at greater mechanical disadvantage relative to internal pressure than a smaller heart).

  40. Major factors determining myocardial contractile state (ie. inotropicity) • Sympathetic nerve impulses (normal) • Circulating catecholamines (normal) • Force-frequency relation (Bowditch, Treppe, Staircase) Normal) • Various natural inotropic agents (normal) • Digitalis, other non-natural inotropic agents (medical) • Anoxia, hypercapnia, acidosis (pathologic) • Pharmacologic depressants (medical / pathologic) • Loss of myocardium (pathologic) • Intrinsic depressants (normal / pathologic) • Attention: Inotropicity (ie. contractility) and strength of contraction are not synonomous. Increased / decreased strength of contraction can be achieved by changing preload(ie. Frank-Starling) with no change in inotropicity. Inotropicity reflects the biochemical state within the muscle (eg. Ca<SUP++< sup>, ATP), not simply the positioning of the thick and thin • myofilaments as determined by stretch.

  41. Figure 2.04. Two Frank-Starling curves demonstrating altered inotropicity; Blue - lower inotropicity; Green - higher inotropicity.

  42. Inotropic agents: • Positive: • Catecholamines (epinephrine, norepinephrine, isoproterenol) • Ca++ • Cardiac glycosides (digitalis) Negative: • Ischemia/hypoxia • Acetylcholine • Heart Failure

  43. Stages of the cardiac cycle

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