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77 Cards in this Set

  • Front
  • Back
What is the relative ion distribution of K, Na, and Ca in a typical cell?
K in > K out
Na and Ca in < Na and Ca out
Na/K Pump
Requires ATP, 2 K in for every 3 Na out
Na/Ca Pump
1 Ca out for every 3 Na in
At rest, the permeability of K is what in relation to Na?
PK+ >> PNa+ by 100x
What ion's potential determines RMP?
Fast type AP occur where?
Atria and Ventricles
Slow type AP occur where?
SA and AV nodes
Phase 0 of Fast Type AP
Rapid depolarization (voltage dependent) due to Na+ entry

1. Fast type Na+ channels open
2. Slow close of activation gates
Phase 1 of Fast Type AP
Small repolarization

1. Outward mov't of K+
2. Inactivation of Na+ channel
Phase 2 of Fast Type AP
Plateau due to:

1. Ca in through L type Ca channels
2. Slow current of Na in through non-tetrodotoxin Na+ channel
3. K+ permeability decreases
Inward Retification
Less outward K+ current b/c K permeability decrease
Phase 3 of Fast Type AP

1. Na and Ca channels inactivated so currents stop
2. Increased permeability of K+
Phase 4 of Fast Type AP
Stable RMP
Absolute Refractory Period
Inactivation of Fast Na channels so Ca can enter, contraction of heart
Slow vs. Fast AP

1. Slower initial depolarization, but spontaneous
2. Lower amplitude overshoot
3. Shorter and less stable plateau phase
4. Unstable RMP
Phases 0-2 of Slow Type AP
Depolarization mainly due to Ca entry
Phase 3 of Slow Type AP

1. Ca and Na channels inactivated
2. Increased permeability of K
Phase 4 of Slow Type AP
Spontaneous depolarization due to:

1. Decreasing K permeability
2. Increasing Ca permeability
3. Increasing Na permeability
Where is the origin of the heart beat?
SA node and potentially AV node
What's norepinephrine's effect on heart rate?
Increase by causing faster phase 4 depolarization (Ca channel opening enhanced)
What's acetycholine's effect on heart rate?
Decreases heart rate by causing slower phase 4 depolarization (K channel opening enhanced)
Describe spread of excitation w/in heart.
1. Atria contract
2. Electrical events reach AV node
3. Conduction slow, ventricular filling
4. Purkinje fibers accelerate excitation to allow for coordinated contraction
P Wave
Atrial depolarization and contraction
QRS Wave
Ventricular depolarization and contraction
T Wave
Ventricular repolarization
What happens w/heart failure?
1. Blood accumulates behind the heart
2. Not enough blood flows out of the heart into the body
Ca enters the cytosol of myocytes from which 2 places?
1. Extracellular space
2. Sarcoplasmic reticulum
In order for the heart to relax, what must Ca do?
Ca must be removed from the cytosol(uphill transport)
When Ca enters the cytosol, what kind of protein does it bind?
Ca binds high-affinity Ca binding E-F PROTEIN
In what kind of cells is diffusion from the extracellular fluid sufficient for contraction?
Embryonic muscle and adult smooth muscle
The sarcoplasmic reticulum includes what 2 distinct regions?
1. Sarcotubular network
2. Subsarcolemmal cisternae
Sarcotubular network
Pumps Ca OUT of the cytosol
Subsarcolemmal cisternae
Transmit signals generated by depolarization of the T-tubules
Transverse tubulues (t-tubules)
Extension of sarcoplasmic reticulum, open to extracellular space, carry AP to inner parts of cell
Special structures formed by t-tubules and subsarcolemmal cisternae
How do AP at cell surface trigger Ca release from SR?
1. T-tubulues open to and communicate w/extracellular space
2. T-tubule membrane propagates AP
Which structures are involved in the external Ca cycle?
Ca in from ECF:
1. L-type Ca channel

Ca out to ECF:
2. Plasma membrane Ca Pump
3. Na/Ca Exchanger

-Na/K ATPase: generates small repolarizing current, helps maintain RMP
Which structures are involved in the internal Ca cycle?
Ca into cytosol from SR:
1. SR Ca Release Channel

Ca into SR from cytosol:
1. SR Ca Pump
Plasma Membrane Ca Pump (PMCA)
Part of external Ca cycle, pumps Ca out into cytosol, requires ATP
Na/Ca Exchanger (NCX)
Part of external Ca cycle, 3 Na in for 1 Ca out (depolarizing effect)
Which external Ca cycle structure has depolarizing effects? What can it cause clinically?
Na/Ca Pump can cause cardiac arrhythmias/sudden cardiac death
Which internal Ca cycle structure is aka ryanodine receptors/feet?
SR Ca release channels
How are SR Ca release channels opened?
By Ca entry from L-type Ca channels
Troponin C
EF protein that binds Ca to initiate muscular contraction
Sarcoplasmic Reticulum Ca Pump (SERCA)
Part of internal Ca cycle, pumps Ca into SR
Regulates SERCA
How does phosphlamban regulate Ca uptake?
If dephosphorylated, SLOWS Ca uptake into SR

If phosphorylated, SPEEDS UP Ca uptake into SR
Stores CA w/in SR
B/w 2 Z lines containing 1 A band and 2 half I-bands
Striations in the sarcomere are a result of what?
Distribution of thick and thin filaments
Cross bridges. How are they in resting vs. active muscle?
Project from THICK filaments

Resting muscle: Perpendicular to thick filaments, not bound to thin filaments.

Active muscle: Row thin filaments toward the center
Which contractile proteins are involved in muscle contraction?
Myosin (thick filament) and Actin (thin filament)
Which regulatory proteins are involved in muscle contraction?
Tropomyosin, Troponin C, Troponin I, and Troponin T
Tropomyosin (TM)
Protein that lies in the groove b/w 2 actin strands
Troponin I (TN-I)
Inhibits actin-myosin interactions when Troponin C is not bound
Troponin C (TN-C)
E-F hand Ca binding protein, binds CA to activate muscle contraction
What happens when TN-C is not bound to Ca?
Active sites on actin are blocked so actin cannot interact w/myosin
Troponin T (TN-T)
Binds TM, TN-C, TN-I to thin filament
Load supported BEFORE contraction
Load supported AFTER contraction
Maximal Afterload
Isometric contraction where muscle can't shorten/no cycling
Zero Afterload
Cross-bridges cycle at maximal rate
What is the effect of increasing the afterload on cardiac efficiency?
Cardiac efficiency decreases
Muscle length is determined by what?
Preload that stretches muscle (direct relationship)
Maximal force is determined primarily by what?
# of actin sites interacting w/myosin...amount of Ca bound to TN-C
Maximal shortening velocity is determined by what?
Actin-myosin cross-bridge turnover rate (myosin heavy chain isoform)
Resting tension of a muscle
Force required to stretch a resting muscle to different lengths
Active or developed tension of a muscle
Tension developed in a muscle when it is stimulated to contract but the length is held constant (the ends are fixed)
At what muscle length is maximum active tension achieved? How does this property affect cardiac muscles?
At an intermediate muscle length (Lmax). Little tension is developed at very short or very long lengths. Cardiac muscle usually operates at lengths much lower than Lmax, so increasing muscle length increases active tension during isometric contraction.
What is the relationship b/w EDV (preload), SW, SV?
Proportional to SW and SV
How is EDV related to muscle length?
Length varies directly with EDV
Afterload can be increased how? What happens to the VFC?
1. Increasing PAd, size, pressure

VFC lower
What are 2 ways you can increase SV for the same PAd?
1. Increase preload
2. Increase contractility
Heart regulation as a result of changing initial muscle length
Heart regulation as a result of change in contractility
According to the Law of Laplace, afterload depends on what 2 factors?
1. pressure
2. size
Starling's Law
Stroke volume increases as cardiac filling increases