Downloaded 78 times
![ Intrinsic ability of cardiac muscle
Also called ‘inotropism’ or ‘inotropy’
Related to the intracellular [Ca2+]
Inotropic agents
◦ positive: increase contractility
◦ negative: decrease contractility](https://image.slidesharecdn.com/cardiaccontractility-130216085108-phpapp01/85/Cardiac-contractility-10-320.jpg)
![ Chronotropy
◦ rate of contraction
◦ also affected by intracellular [Ca2+]
Dromotropy
◦ rate of impulse conduction
◦ noted particularly at AV node](https://image.slidesharecdn.com/cardiaccontractility-130216085108-phpapp01/85/Cardiac-contractility-11-320.jpg)
![ Increased intracellular [Ca2+]
◦ increased heart rate
◦ cardiac glycosides (e.g. digoxin)
Stimulation of β1-adrenergic receptor
◦ sympathomimetic agents
◦ catecholamines](https://image.slidesharecdn.com/cardiaccontractility-130216085108-phpapp01/85/Cardiac-contractility-12-320.jpg)
Uploaded byKiran Goushika
Cardiac contractility
The document discusses cardiac electrophysiology and contractility. It describes the pacemaker potential and automaticity of the sinoatrial node, which allows it to initiate action potentials without external stimulation at a rate of 100 beats per minute. It also discusses the conduction of action potentials through the heart via the atrioventricular node, bundle of His, and Purkinje fibers. Contraction is triggered by increases in intracellular calcium levels. The cardiac action potential is longer than in skeletal muscle, lasting 200-300 milliseconds, which allows time for relaxation between contractions.
More Related Content
Similar to Cardiac contractility
Cardiac contractility
- 1.
- 2. Cardiac Electrophysiology Cardiac Contractility
- 3. The science ofelucidating ,diagnosing, and treating electrical activities of heart.
- 4. Actions potentials ◦ SA node ◦ Cardiac muscle (atria, ventricles & Purkinje fibers) Channels ◦ Ca2+ channel ◦ β-adrenergic receptor ◦ Na+/K+-ATPase
- 5. Phase 0 Phase 3 0 mV -50 mV -70 mV Ca2+ Phase 4 Phase 4
- 6. Pacemaker ofthe 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. Phase 0 Phase 1 Phase 2 +30 mV 0 mV Phase 3 Ca 2+ -70 mV -90 mV Resting Potential Phase 4
- 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 receptor Na+/K+ ATPase Na+/Ca2+ Antiporter Representative Cardiac Cell
- 9. The intrinsic abilityof heart to contract
- 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. Chronotropy ◦ rate of contraction ◦ also affected by intracellular [Ca2+] Dromotropy ◦ rate of impulse conduction ◦ noted particularly at AV node
- 12. Increased intracellular [Ca2+] ◦ increased heart rate ◦ cardiac glycosides (e.g. digoxin) Stimulation of β1-adrenergic receptor ◦ sympathomimetic agents ◦ catecholamines
- 14. 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
- 15. 2 K+ Phase 2 3 Na+ Ca2+ Ca2+ 3 Na+ Ca2+ Ca2+ SR (Mitochondria) Ca 2+ Ca2+ Ca2+ Ca2+ Ca2+ Cell Electrophysiology
- 16. ATRIAL MUSCLE VENTRICULAR MUSCLE SPECIALISES EXCITATORY &CONDUCTIVE MUSCLE FIBERS
- 18. Interconnected byintercalated discs and form functional syncytia Withinintercalated discs – two kinds of membrane junctions ◦ Desmosomes ◦ Gap junctions
- 20. 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
- 21. Autorhythmicity: The abilityto initiate a heart beat continuously and regularly without external stimulation Excitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potential Conductivity: The ability to conduct excitation through the cardiac tissue Contractility: The ability to contract in response to stimulation
- 22. Definition: the abilityof 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
- 23. 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
- 24. SITE SA node acts as heart RATE(Time/minu pacemaker because it has the te) fastest rate of generating action SA Node 100 potential Nerve impulses from AV Node 40-60 autonomic nervous system and hormones modify the timing and strength of each heart beat but do AV bundle, bundle 20-35 not establish the fundamental branches,& Purkinje rhythm. fibres
- 25. Definition: The abilityof 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
- 28. 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
- 29. Definition: ability of cardiac muscle to contract in response to stimulation
- 30. Similar to that in skeletal muscles
- 31. Definition: property by which excitation is conducted through the cardiac tissue
- 33. 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
- 34.
Editor's Notes
- #14 Therapeutic: Digoxin inhibits Na+/K+ ATPase (exchange pump) Increased intracellular [Na+], and increased extracellular [K+] Leads to decreased Na+/Ca++ exchange Which leads to increased intracellular [Ca++] Leading to increased contractility Toxicologic Excessive intracellular [Ca++] Less negative membrane potential (closer to threshold = depolarization) Increased automaticity Tachydysrhythmias
- #15 Therapeutic: Digoxin inhibits Na+/K+ ATPase (exchange pump) Increased intracellular [Na+], and increased extracellular [K+] Leads to decreased Na+/Ca++ exchange Which leads to increased intracellular [Ca++] Leading to increased contractility Toxicologic Excessive intracellular [Ca++] Less negative membrane potential (closer to threshold = depolarization) Increased automaticity Tachydysrhythmias
- #22 Therapeutic: Digoxin inhibits Na+/K+ ATPase (exchange pump) Increased intracellular [Na+], and increased extracellular [K+] Leads to decreased Na+/Ca++ exchange Which leads to increased intracellular [Ca++] Leading to increased contractility Toxicologic Excessive intracellular [Ca++] Less negative membrane potential (closer to threshold = depolarization) Increased automaticity Tachydysrhythmias