Physiology 3120 Lecture Notes - Sliding Filament Theory, Intercalated Disc, Sinoatrial Node

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Published on 26 Nov 2011
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Human Physiology
Wednesday, January 13, 2010
“CV V”
Function of Myocardial Cells
Looking at microscopic level (cellular, molecular, etc.)
Heart beat = most important life-sustaining event; heart is first organ formed during embryogenesis
Three types of muscle fibres
1. Atrial**
2. Ventricular**
3. Excitatory & conductive
Not much contractile capacity
Rhythmicity (excitatory system to generate impulses)
Rapid conduction (conduct impulses)
In skeletal muscle, muscle fibres function independently of each other; cardiac muscle fibres are
interconnected & form a system (i.e. syncytium)
Where two fibres meet, membrane folds in region called intercalated disc
Two functional syncytium in heart
1. Atrial syncytium
Contract before the ventricles because of the impulse generated in the SA node
(must conduct down into ventricles)
2. Ventricular syncytium
**have contractile properties like skeletal muscle (i.e. sliding filament theory; however, there are major
differences [i.e. troponin])**
Impulse generated at sinus node (located just under vena cava in right atrium)
The “pacemaker” of the heart
Impulse generation in this area occurs faster than elsewhere in the heart
Special properties (all of which work to depolarize the SA node cells)
Greater Na permeability
K permeability declines during diastole (more positive charges inside cell)
Slow inward Ca current
No “STABLE” resting membrane potential
During diastole, the SA node slowly depolarizes (called the pre-potential); doesn’t
hyperpolarize as much as in other cells (-55 to -65 mV)
Threshold is about -40mV; opens slow sodium & calcium channels (different from V.G.
channels); once membrane potential reaches a peak, the sodium/calcium channels close and
potassium permeability increases
Impulse conduction
Spreads quickly through atria (both) & reaches the AV node, where it is delayed again (low
conduction velocity)
AV bundle conducted into the Bundle of His and then into Purkinje fibres (highest conduction
velocity)
Get complete excitation of ventricle in 60ms; duration of ventricular contraction lasts 300ms
Ensures that the entire ventricle contract at once
Improper conduction can give rises to arrhythmia, or an abnormal heartbeat
Ways to adjust the heart rate
Change threshold of excitation in SA node
Change slope of pre-potential by further decreasing K permeability
Change degree of hyperpolarization (i.e. hyperpolarize it less)
Action potentials in heart regions
Slope of AP in SA and AV nodes much lower than in other areas (i.e. slower conduction)
APs in SA & AV nodes are slow-response APs (slow rate of depolarization)
After the Bundle of His, the APs reach a plateau, but the regions proximal to these ones show no
plateau
APs and refractory periods (ventricular muscle)
RMP of -90mV (much lower than S.A.)
Depolarization due to opening of fast Na channels (MP becomes positive)
Short-lived repolarization due to closure of Na channels & small amount of chloride
entering the cell
Opening of Na channels initiates opening of SLOW Ca channels (slow-starting, long-
lasting); K ions also moving into the cell; this balance between ion flow creates the
plateau observed in the AP
Repolarization results when Ca channels close and K continues to leak out
Supernormal period if the muscle gets excited during this time, the ventricle can
undergo ventricular fibrillation (a rapid irregular rhythm)
Much longer than a typical AP (about 250ms)