Physio Ch 10 Flashcards
Under normal conditions, atria contract ___ ahead of ventricles
1/6 of a second
conduct impulses from the sinus node to the atrioventricular (A-V) node
internodal pathways
conducts impulses from the atria into the ventricles
A-V bundle
conduct the cardiac impulses to all parts of the ventricles
right and left bundle branches of Purkinje fibers
where impulses from the atria are delayed
before passing into the ventricles
AV node
a small, flattened, ellipsoid strip of specialized cardiac muscle
SA node
Located superior posterolateral wall of right atrium below and slightly lateral to the opening of the superior vena cava
SA node
a process that can cause automatic rhythmical discharge and contraction
self-excitation
resting membrane potential of the sinus nodal fiber between discharges
-55 to -60 mV
RMP of ventricular muscle fiber
-85 to -90
Why does SA node have lesser RMP or negativity?
Due to cell membrane’s natural leak to sodium and calcium ions (positive ions go inside the fibers)
What are the 3 types of membrane ion channels present in the cardiac muscle?
(1) fast sodium channels
(2) slow sodium-calcium channels
(3) potassium channels
Which channel is responsible for the rapid upstroke spike of the action potential observed in ventricular muscle
fast sodium channels
Which channel is responsible for the plateau of the ventricular action potential
slow sodium-calcium channel
Responsible for returning the cell membrane’s potential to its resting level
potassium channels
resting potential of SA fibers gradually rises and becomes less negative between each ___ ?
2 heartbeats
threshold voltage of SA fibers
-40 mV
What is responsible for sinus nodal fibers self-excitation?
Inherent leakiness to sodium and calcium ions
What are the 2 events that cause the sinus nodal fibers not remain depolarized all the time, despite its leakiness to sodium and calcium?
- Sodium-calcium channels become inactivated within 100-150 secs after opening
- Many potassium channels open
Briefly summarize the process of self-excitation to re-excitation process of SA fibers.
- self-excitation to cause the action
potential - recovery from the action potential
- hyperpolarization after the action potential is over
- drift of the “resting” potential to threshold
- re-excitation to elicit another cycle
small bands of atrial fibers that passes through the anterior walls of the atria
to the left atrium
Anterior interatrial band
What delays the transmission of conduction of the atria to the ventricles?
A-V node and adjacent conductive fibers
located in the posterior wall of the right
atrium immediately behind the tricuspid valve
A-V node
What causes the slow conduction in the transitional, nodal, and penetrating A-V bundle fibers?
diminished gap junctions
transmit action potentials at a velocity of 1.5 to 4.0m/sec
Purkinje fibers
What allows rapid transmission of action potentials by Purkinje fibers?
High permeability of gap junctions at the intercalated discs
acts as an insulator to prevent passage of
the cardiac impulse between atrial and ventricular muscle through any other route besides forward conduction through the A-V bundle itself
continuous fibrous barrier
discharge at an intrinsic rhythmical rate
of 40 to 60 times per minute when not stimulated from outside source
A-V nodal fibers
Why does the sinus node rather than the A-V
node or the Purkinje fibers control the heart’s rhythmicity?
Discharge rate of the sinus node is considerably faster than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers.
its rate of rhythmical discharge is faster than
that of any other part of the heart
SA node
What is an ectopic pacemaker?
A pacemaker elsewhere than the sinus node
responsible for abnormal sequence of contraction of the different parts of the heart and can cause significant debility of heart pumping
ectopic pacemaker
delayed pickup of the heartbeat due to A-V block
Stroke-Adams syndrome
What are the 2 major effects of acetylcholine released on the vagal endings to the heart?
- Decreases rate of rhythm of the sinus node
- Decreases the excitability of the A-V junctional fibers between the atrial musculature and the A-V node
It is when vagi stops or block the transmission of cardiac impulse from atria to ventricles, but some areas of Purkinje fibers develops a rhythm of its own and causes ventricular contraction
Ventricular escape
Effect of Sympathetic Stimulation on Cardiac Rhythm and Conduction (3)
- Increases the rate of sinus nodal discharge
- Increases the rate of conduction and level of excitability
- Increases the force of contractions of all the cardiac musculature
hormone released by sympathetic nerves to increase the overall activity of the heart
norepinephrine
