Physiology #20: Cardiac Electrophysiology
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What is the function of the atria?
Atria: function as primer pumps for the ventricles
What is the function of the ventricles?
Ventricles serve as a power pump to supply the main force that propels blood through the systemic and pulmonary circulations
What are the types of Cardiac cells?
- Contracting and Conducting cells
- Contractile cells: the majority of the atrial and ventricular tissues.
- -Are the working cells of the heart.
- - AP lead to contraction and generation of F or P
- Conducting cells: Tissues of the SA node, atrial intermodal tracts, AV node, bundle of His, Purkinje system.
- -specialised muscle cells that do NOT generate F
- -function to rapidly spread AP over the entire heart
- - also capable of generating AP spontaneously
- cardiac muscle is striated (like skeletal muscle) and contains actin and myosin filaments
- cells are tightly bound for propagation of AP spread
- via GAP JXNS
Who is running the show in heart contraction?
Where are conduction impulses generated and what path do they take?
- Normally impulses are generated in the SA node
- they travel from the SA node to the AV node, down the bundle branches of His and into the purkinje fibers in the walls of the ventricles
- sinoatrial node
- serves as the pacemaker of the heart
- APs that drive the heart are initiated here, in the wall of the R atrium
- AP spread from the SA node to the R and L atria via intermodal tracts
- AP is also conducted to AV node
- Atrioventricular node
- *slows conduction velocity to allow atria to contract first and prime
- slow conduction through the AV nodes ensures that the ventricles have time to fill with blood before they are activated and contract
- Atria have time to act as primer pumps to top up the ventricular V before they contract
Bundle of HIS, Purkinje System, ventricles
- specialised conduction system of ventricles
- conduction is extremely fast, rapidly distributes the AP to the ventricles AP spread from one ventricular cell to the next through low resistance connection between cells
- allows for coordinated contraction and ejection of blood
What makes Cardiac APs?
- cardiac AP results form time-dependent changes in the permeability of cardiac muscle cell membranes to Na+, Ca++, and K+
- The permeability changes that occur are referred to as phases 0-4 (*5 phases) of the AP
- AP are slightly different in the different areas of the heart ie ventricles, atria, and SA node
- shape depends on what that part of the heart is designed to do
- ventricles: have a longer wave form than atria
- atria shorter wave form, but atria and ventricles are similar
- SA node looks much diff
- membrane potential of cardiac cells is determined by the relative permeabilities / conductances of different ions
- when the membrane is permeable, ions flow down their electrochemical gradients toward their "equilibrium potentials"
- Current = driving F x conductance
Resting membrane potentials of cardiac cells are primarily determined by ******
What are changes in membrane potentials due to?
Changes in membrane potentials are due to flow of ions into or out of cells
depolarization means the membrane potential has become less negative (net movement of positive charge into the cell)
hyperpolarization means the membrane potential has become more negative (net movement of positive charge out of the cell)
Differences in AP in cardiac cells compared to nerve and skeletal muscle cells
- very fast in nerve and muscle (1-2 ms)
- very slow in cardiac (atria: 150ms, ventricles 250ms, purkinje 300ms)
- cardiac cells have longer refractory periods ( when cant be activated by another AP) thann nerve and skeletal tissue
- ***have a plateau phase to their AP (not seen in nerve and skeletal muscle)
-resting transmembrane potential
- atria, ventricles, purkinke fibers
- *normally these cells have a resting transmembrane potential of - 85mV (aka phase 4)
- ***IN NONPACEMAKER CELLS, PHASE 4 IS CONSTANT DURING DIASTOLE (there is no change in membrane potential)
- cells remain at rest until activated by a propagated cardiac impulse or external stimulus
- Phase 0 = "upstroke"
- Phase of Rapid Depolarization
- result of transient increase in Na+ conductance when voltage gated Na channels open
- Na+ channels open briefly then close, so membrane potential only depolarizes to a value of +20mV not to the equilibrium potential of Na
- Initial Repolarization
- net outward current of positive charge, causing repolarization
- cease of inward flow of Na+ as channels close
- outward flow of K+ (large K+ gradient) current is caused by chemical and electrical (+ charge inside cell) driving forces
- Long period of relatively stable, depolarized membrane potential
- More obvious in ventricular and purkinje fibers than atrial fibers
- results in a sustained period of ventricular contraction to pump blood out of the heart
- characterised by a slow inward flow of Ca++ ions and slow outward current of K+ ions (NO NET movement of charge across the membrane - the curve is flat)
What is Ca++ important for?
Ca++ is important for myocardial cell excitation-contraction coupling and muscle contraction AND phase 2 of AP (long ventricular contraction)
- Phase of rapid repolarization
- outward currents are greater than inward currents
- decreased Ca++ movement into cells, increased K+ movement out of cells (to re set to threshold)
- "resting membrane potential"
- Inward and outward currents are equal
- constant and ready to contract
- small amount of K+ movement out of cell
- small amount of Na+ and Ca++ movement into cells
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