L15/16 Cardiac Electrophysiology And Excitation-Contraction Flashcards
(39 cards)
Cardiac muscle
Striated
ANS involuntary
Multi-nucleated
Junctions
Large mitochondria
Intercalated discs
Connect adjacent cardiac muscle fibers and form function syncytium
Two kinds of membrane junctions within them:
Desmosomes-mechanical junctions
Gap junctions- electrical junctions
Cardiac muscle looks similar to
Skeletal muscle
Sarcolemma
T-tubules
SR sacks
Sequence of electrical events in the heart
SA node AV node Bundle of His Bundle branches (left and right) Purkinje fibers
Only way to guarantee ventricles aren’t contracting while atria are
Isolating electrical activity from one part of the heart from the other
Controls when ventricles get activated compared to atria
Bundle of his
On pathway between atria and ventricles
Delay in conduction of activity btw AV node and ventricles
Conduction of the cardiac AP
Atria - fast
AV node - slows down
His-purkinje - fastest
Ventricle - back to atria velocity
Due to how fast AP can depolarize and depolarize
AV node delay
AV node to bundle of his is Only point of electrical contact btw atria and ventricle
Very slow conduction
Allows adequate time for ventricular filling btw beats
Essential to synchronize atria and ventricular contractility
Purkinje fibers
Mesh of specialized fibers with very fast conduction
Rapidly spread impulse throughout much of left and right ventricles
Allows for efficient contraction and ejection of blood
Overdrive suppression
Phenomenon by which SA node drives heart rate and suppresses the latent pacemakers
Wait for impulses to be retrieved
SA node has
Fastest intrinsic firing rate
Damage to SA node, AV node may have control over heart rate
Ectopic pacemaker (ectopic focus)
Occurs when the latent pacemakers have an opportunity to drive the heart rate ONLY if
SA node firing rate decreases (vagal stimulation)
SA node firing stops completely (SA node destroyed, removed, etc)
Intrinsic firing of latent pacemakers become faster
Conduction of APs from SA node is blocked by disease
Types of myocardial cells
Pacemaker (nodal) cells
Conductile cells
Contractile cells
Pacemaker (nodal) cells
Pacemaker activity
Slow action potentials
SA node (primary) AV node
Conductile cells
Rapid spread of electrical signal
FAST AP
bundle of his
Purkinje fibers
No myosin or action
Contractile cells
Contraction (pumping)
FAST AP
Ventricular and atrial cells
Contain myosin and action
Phases of fast AP
Phase 0: upstroke (similar to skeletal muscle AP) fast inward Na+ current
Phase 1: early repolarization
Transient K+ channels (Ito; outward)
Phase 2: plateau phase
L-type Ca2+ channel inward (depolarizes) and K+ (Ito, Ik, Ik1) currents outward (hyperpolarize)
Phase 3: repolarization
turn-off Ca current and increases K current
Phase 4: resting potential
Caused by large background K current
Resting membrane potential of heart
-90
Due to many more leaky K channels (high permeability to K at rest)
Phases of slow AP
Phase 0: upstroke
L-type Ca channel ( NOT Na - capacity lower)
Phase 1 and 2: absent
Phase 3: repolarization
K current
Phase 4: pacemaker potential (spontaneous depolarization)
“Funny” Na current (If) and a T-type (transient) Ca current
Relationship of AP and refractory period to the duration of the contractile response in cardiac muscle
Because long refractory period occurs in connecting with prolonged plateau phase
Summation and that is of cardiac muscle is impossible
Ensures alternate periods of contraction and relaxation which are essential for pumping blood
Excitation-contraction coupling in cardiac contractile cells
- Excitation AP causes depolarization of the membrane (Travels down T tubule)
- Entry of small amount Ca from ECF through L-type Ca channels
- Ca enters cell
- Ca-induced Ca release from SR (essential)
- SR releases large amount Ca through ryanodine receptors. Cytosolic Ca levels increase
- Ca binds troponin-tropomyosin complex in thin filaments pulled aside
- Cross bridge cycling btw thick and thin filaments
- Contraction
Ca induced Ca release in cardiac muscle
Ca enters through L type Ca channel
Ryr receptor is close proximity to L type Ca channel but not physical connection
Necessary for contraction
Mechanism for decreasing intracellular Ca in cardiac muscle
Decrease in contractile force occurs when conc intercellular Ca decreases
Cytosolic Ca conc decrease by:
SR Ca ATPase (SERCA)
Sarcolemmal Na/Ca exchanger (NXC)
Sarcolemmal Ca ATPase
Need Na/K ATPase for NCX
Length tension relationship in cardiac muscle
Neither summation nor recruitment occurs
Force contraction is altered in others ways
Does not normally function at peak of Lo
Rather works in ascending limb
stretching cardiac muscle fibers (to a point) increase contraction
Force developed by contraction depends on initial fiber length
