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Cardiac contractility

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Cardiac contractility

  1. 1. Kiran Goushika
  2. 2.  Cardiac Electrophysiology Cardiac Contractility
  3. 3. The science of elucidating ,diagnosing, andtreating electrical activities of heart.
  4. 4.  Actions potentials ◦ SA node ◦ Cardiac muscle  (atria, ventricles & Purkinje fibers) Channels ◦ Ca2+ channel ◦ β-adrenergic receptor ◦ Na+/K+-ATPase
  5. 5. Phase 0 Phase 30 mV-50 mV-70 mV Ca2+ Phase 4 Phase 4
  6. 6.  Pacemaker of the heart Unstable resting potential ◦ Exhibits automaticity ◦ AV node & His-Purkinje system are latent pacemakers Phase 1 & 2 are not present in pacemaker action potentials
  7. 7. Phase 0 Phase 1 Phase 2 +30 mV 0 mV Phase 3 Ca 2+ -70 mV -90 mV Resting PotentialPhase 4
  8. 8. Voltage dependent Voltage dependent Na channel + channel + L-type Ca2+ channel L-type 2+ channel Na+/K+ ATPase Na+/K+ ATPase 2K + 3 Na+ K+ channel(s) + channel(s) Ca2+ 3 Na+ β-adrenergic receptor β-adrenergic receptor Na+/Ca2+ exchanger Na+/Ca2+ exchanger SR (Mitochondria) Heart muscle Heart muscle Ryanodine receptor Ryanodine receptorNa+/K+ ATPaseNa+/Ca2+ Antiporter Representative Cardiac Cell
  9. 9. The intrinsic ability of heart to contract
  10. 10.  Intrinsic ability of cardiac muscle Also called ‘inotropism’ or ‘inotropy’ Related to the intracellular [Ca2+] Inotropic agents ◦ positive: increase contractility ◦ negative: decrease contractility
  11. 11.  Chronotropy ◦ rate of contraction ◦ also affected by intracellular [Ca2+] Dromotropy ◦ rate of impulse conduction ◦ noted particularly at AV node
  12. 12.  Increased intracellular [Ca2+] ◦ increased heart rate ◦ cardiac glycosides (e.g. digoxin) Stimulation of β1-adrenergic receptor ◦ sympathomimetic agents ◦ catecholamines
  13. 13.  Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum ◦ Ca2+ induced Ca2+ release leads to cross-bridge cycling and contraction
  14. 14. 2 K+Phase 2 3 Na+ Ca2+ Ca2+ 3 Na+ Ca2+ Ca2+ SR (Mitochondria) Ca 2+ Ca2+ Ca2+ Ca2+ Ca2+ Cell Electrophysiology
  15. 15.  ATRIAL MUSCLE VENTRICULAR MUSCLE SPECIALISES EXCITATORY &CONDUCTIVE MUSCLE FIBERS
  16. 16.  Interconnected by intercalated discs and form functional syncytia Withinintercalated discs – two kinds of membrane junctions ◦ Desmosomes ◦ Gap junctions
  17. 17.  Exhibit branching Adjacent cardiac cells are joined end to end by specialized structures known as intercalated discs Within intercalated discs there are two types of junctions ◦ Desmosomes ◦ Gap junctions..allow action potential to spread from one cell to adjacent cells. Heart function as syncytium when one cardiac cell undergoes an action potential, the electrical impulse spreads to all other cells that are joined by gap junctions so they become excited and contract as a single functional syncytium.Atrial syncytium and ventricular syncytium
  18. 18. Autorhythmicity: The ability to initiate a heart beat continuously and regularly without external stimulationExcitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potentialConductivity: The ability to conduct excitation through the cardiac tissueContractility: The ability to contract in response to stimulation
  19. 19. Definition: the ability of the heart to initiate its beat continuously and regularly without external stimulation myogenic (independent of nerve supply) due to the specialized excitatory & conductive system of the heart ↓ intrinsic ability of self-excitation (waves of depolarization) ↓ cardiac impulses
  20. 20.  Autorythmic cells do not have stable resting membrane potential (RMP) Natural leakiness to Na & Ca→ spontaneous and gradual depolarization Unstable resting membrane potential (= pacemaker potential) Gradual depolarization reaches threshold (-40 mv) → spontaneous AP generation
  21. 21. SITE SA node acts as heart RATE(Time/minu pacemaker because it has the te) fastest rate of generating actionSA Node 100 potential Nerve impulses fromAV Node 40-60 autonomic nervous system and hormones modify the timing and strength of each heart beat but doAV bundle, bundle 20-35 not establish the fundamentalbranches,& Purkinje rhythm.fibres
  22. 22. Definition: The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an AP  AP initiated by SA node→travels along conductive pathway→ excites atrial & ventricular muscle fibres
  23. 23.  Long refractory period (250 msec) compared to skeletal muscle (3msec) During this period membrane is refractory to further stimulation until contraction is over. It lasts longer than muscle contraction, prevents tetanus Gives time to heart to relax after each contraction, prevent fatigue It allows time for the heart chambers to fill during diastole before next contraction AP in skeletal muscle : 1-5 msec AP in cardiac muscle :200 -300 msec
  24. 24.  Definition: ability of cardiac muscle to contract in response to stimulation
  25. 25.  Similar to that in skeletal muscles
  26. 26.  Definition: property by which excitation is conducted through the cardiac tissue
  27. 27.  Cardiac impulse originates at SA node Action potential spreads throughout right and left atria Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers) Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling) Impulse travels rapidly down interventricular septum by means of bundle of His Impulse rapidly disperses throughout myocardium by means of Purkinje fibers Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions
  28. 28. PROFESSOR: Maka
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