Cardiac Physiology: APs, RMP, and Conduction System Flashcards
What are the structures that make up the conduction system?
In order of normal propagation: SA Node Inter-atrial Pathway AV Node Common AV Bundle (Bundle of His) R & L Bundle Branches Purkinje Fibers
What are some functional characteristics of the conduction system of the heart?
SA node - pacemaker of the heart
Anterior interartrial myocardial band ~1m/s
(SA node -> L atrium)
AV node - generally delays impulse transmission between atria and ventricles
3 functional regions
1. AN region - transitional zone between atrium and the node - longer conduction path
2. N region - midportion of the AV node - slows conduction velocity
3. NH region - nodal fibers merge with Bundle of His
Bundle of His and Purkinje fibers
What is the relative rate of conduction velocity and pacemaker activity of the components of the conduction system of the heart?
Conduction velocity Slowest: (small diameter, increased resistance) AV node SA node Ventricular myocytes
Fastest: (larger diameter, decreased resistance)
Purkinje Fibers
Bundle Branches
Explain the intrinsic pacemaker activity of the heart.
SA node (pacemaker) 60-100 bpm
AV junction 40-60 bpm
Purkinje fibers 20-40 bpm
What does AV block or prolonged nodal delay cause?
Ventricular bradycardia
- distal pacemaker sites generating the ventricular rhythm
- secondary pacemaker sites have a lower intrinsic rate than the SA node
What does SA nodal failure result in?
Bradycardia
- SA nodal failure unmasks slower latent pacemakers in AV node or ventricular conduction system
- creates escape beats or rhythms
How do gap junctions allow the cardiac myocytes to work as a functional syncytium?
Gap junctions are low resistance electrical connections that allow AP propagation to adjacent cells
- if one cardiac cell depolarizes, all will eventually depolarize
What is the role of extracellular Ca++ release in initiating cardiac contraction?
Initial influx of extracellular Ca++ is required for release of additional Ca++ from sarcoplasmic reticulum
2 Sources of Ca++ for Cardiac Contraction
1. Ca++ influx from ECF via VG L-type Ca++ channels during long plateau phase of cardiac mm
- Ca++ induced (Ca++ dep) Ca++ release from the SR via Ca++ release channels (RYR)
- release of Ca++ from the SR also req
- amount of Ca++ from ECF alone is too small to promote actin-myosin binding
- Ca++ influx from the ECF triggers Ca++ release from the SR
What is the process/pathway from AP in cardiac mm cell all the way to contraction?
- AP in cardiac contractile cell
- AP travels down T-tubules
- Entry of small amount of Ca++ from ECF
- Release of large amounts of Ca++ from sarcoplasmic reticulum
- Increased cytosolic [Ca++]
- Troponin-tropomyosin complex in thin filaments pulled aside
- Cross-bridge cycling between thick and thin filaments
- Thin filaments slide inward between thick filaments
- Contraction
What is the all-or-none law for the heart?
Normally, all cardiac cells contract or none do
- due to functional syncytium
Atria and ventricles each form a fxnal syncytium, contract as separate units
How is the RMP of a cardiac cell restored?
Removal of Ca++ to ECF
- 3Na+ - 1 Ca++ antiporter (sarcolemma)
- higher Na+ in ECF, Na+ gradient powers Ca++ removal - Ca++ Pump (sarcolemma)
- ATP used to pump out Ca++ into ECF
Sequestering Ca++ into the SR
- SR Ca++ pump (SERCA)
- reg by phospholamban
What is the ion distribution of a cardiac cell? What are the main contributors to RMP?
In:
High K+
low Ca++
low Na+
Out:
low K+
High Ca++
High Na+
K+ and Ca++ are main contributors to RMP
- Na+ is main determinant in upstroke of AP, but contributes very little to RMP - gNa is very small in resting cell, Vm not significantly affected
What are the general currents and phases associated with slow-response action potentials?
Characterized by rate of depolarizing upstroke - slower, with a more gradual slope
(phase 0)
- mediated by SA and AV nodes
Has gradual upstroke
No early repolarization, absent plateau (phases 1 & 2)
Less distinct transition from plateau to final repolarization (phase 3)
No true resting potential (phase 4) ~-40mV
Fastest conduction velocities
- conduction blocks most likely to occur
What are the general phases of cardiac APs?
0 - rapid depolarization 1 - early rapid repolarization 2 - plateau 3 - final rapid repolarization 4 - resting potential
What are the general currents and phases associated with fast-response action potentials?
Characterized by rate of depolarizing upstroke - very fast, almost immediate
Present in atrial, ventricular myocytes, & Purkinje fibers
0- very rapid, immediate upstroke 1 - early, partial repolarization 2- plateau 3- final repolarization - fairly rapid 4 - resting potential ~ -70 mV
Fast has greater slope of upstroke, AP amplitude and extent of overshoot
- slower conduction velocity though
Fast has quicker recovery from refractoriness, can respond to greater AP firing rates
What is the current of Na+ responsible for in APs?
Rapid depolarizing phase of atrial mm, ventricular mm, and Purkinje fibers
Channels closed at negative RMPs
Rapidly activate when memb depolarizes to threshold
Influx of Na+ resp for rapid AP upstroke in phase 0
Inactivation gates close when memb depolarizes
What is the current of Ca++ responsible for in APs?
Rapid depolarizing in AV and SA nodes
Plateau phase of fast-response APs
Triggers contraction in all contractile cardiomyocytes
- contributes to pacemaker activity
- contributes to upstroke in phase 0
Ca++ channels closed at negative RMP
- activate at more + voltages
- inactivate at slower than Na+ channels
- Ca++ entering through L-type channels triggers release of Ca++ from SR in atrial and ventricular mm
Nodal cells: slower conduction velocity because the smaller Ica depolarizes adjacent cells more slowly
Fast
- smaller Ca++ influx adds to Na+ influx in phase 0 upstroke
-
What is the current of K+ responsible for in APs?
Repolarizing phase in all cardiomyocytes
What is the pacemaker/funny current’s role in APs?
Pacemaker activity (slow depolarization phase) in SA and AV nodal cells and sometimes Purkinje fibers
Funny channel - nonspecific cation channel, mostly N+ current
- activated on hyperpolarization
- non-specific: increases Na+ and K+ currents
Increased Na+ resp for ini of slow depolarization phase
What are some characteristics of atrial muscle APs?
AP duration shorter
- greater efflux of K+ during plateau phase
APs spread directly from cell-to-cell among cardiac myocytes within each atrium
No pacemaker activity in normal atrial mm
What are some characteristics of ventricular muscle APs?
3 time and VG currents: Ina, Ica, Ik
No pacemaker activity in normal ventricular mm
Rapid upstroke from threshold
Prolonged plateau phase
AP duration varies among ventricular cells
- differences in the delayed rectifier K+ currents
What are some characteristics of Purkinje fiber APs?
4 time and VG-dep currents: Ina, Ica, Ik, If
Typically exhibit fast response APs
Normally BB currents activate Purkinje fibers
- rapid upstroke mediate by Ina and Ica
Rapid AP conduction velocity due to large cell diameter and Ina
Long refractory periods
- limits conduction of PACs to ventricles
Slowest intrinsic pacemaker rate
- become fxnal pacemakers only if all nodes fail
- spontaneous purkinje fiber act may activate ventricles, but slowly and unreliably
Fast and Slow Response APs
- slow pacemaker depolarization (phase 0) that depends on If
- unreliable pacemakers due to low rate of pacemaker depolarization
What does the P wave represent?
Represents atrial depolarization
doesn’t include atrial REpolarization, which is ‘buried’ in the QRS complex
What does the PR interval represent?
Interval from the beginning of the P-wave to the beginning of the Q-wave
Represents the initial depolarization of the ventricles
