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Differentiate ventricular cardiac action potential to sinoatrial node potential. What are the
key differences?
Ventricular action potential has stable resting membrane potentials of about −90 millivolts
(mV). This value approaches the K+ equilibrium potential. Action potentials are of long duration,
especially in Purkinje fibers, where they last 300 milliseconds (msec). Its phases are: phase 0
is depolarization, phase 1 is initial repolarization, phase 2 is a plateau, phase 3 is rapid
repolarization and phase 4 is the resting potential. The different phases depend on the opening
and/or closure of specific ion channels.
While Sinoatrial nodal action potential has an unstable resting potential. Its phases are: (1)
Phase 0 is the upstroke of the action potential caused by an increase in Ca2+ conductance. (2)
phase 3 is repolarization. Lastly, (3) phase 4 is slow depolarization that accounts for the
pacemaker activity of the SA node (automaticity). It is caused by an increase in Na+
conductance. phases 1 and 2 are not present in sinoatrial nodal action potential.
What is automaticity, and how does it differ from excitability? How do derangements of
these properties contribute to arrhythmias?
Automaticity is the property of cardiac cells to generate spontaneous action potentials. While
excitabity is the ability of cardiac cells to initiate action potentials in response to inward,
depolarizing current. Abnormal automaticity, that causes arrhythmias, occurs by changing the
resting membrane potential of the cell, bringing it closer to the threshold depolarization. This
mechanism is caused by either Na+ or Ca2+ inward current and sometimes a mixture of both.
Triggered activity also causes arrhythmias. This is caused by afterdepolarizations that may
trigger action potentials. An action potential which is engendered by an after depolarization is
referred to as triggered action potential. Such action potentials cause extrasystoles (extra
heartbeats that fall in between the normal beats). The extrasystoles might induce another
arrhythmia mechanism (re-entry) which may cause persistent arrhythmia. Reentrant
arrhythmias occur when a cardiac impulse traverses a loop of cardiac fibers and reenters
previously excited tissue, when the impulse is conducted slowly around the loop, and when the
impulse is blocked unidirectionally in some section of the loop.
How are the concepts of preload and afterload, developed for skeletal muscle, applied to the
contraction of the heart?
For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when
the ventricle has become filled. The end-diastolic volume is related to right atrial pressure.
When venous return increases, end-diastolic volume increases and stretches or lengthens the
ventricular muscle fibers. While the afterload is the amount of pressure that the heart needs to
exert to eject the blood during ventricular contraction. Increases in aortic pressure cause an
increase in afterload on the left ventricle. On the hand, Increases in pulmonary artery pressure
cause an increase in afterload on the right ventricle.
What is the role of Ca++ in excitation-contraction coupling?
In excitation-contraction coupling, depolarization of the T tubules opens Ca2+ release channels
causing release of Ca2+ from the SR into the intracellular fluid. Ca2+ binds to troponin C on the
thin filaments, causing a conformational change in troponin that moves tropomyosin out of the
way. This activates cross-bridge cycle (contraction) and it will continue to repeat as long as Ca2+
is bound to troponin C. Relaxation occurs when Ca2+ is reaccumulated by the SR Ca2+ -ATPase
(SERCA). In short, calcium signals activate contraction-relaxation cycle.
What is the pressure-volume loop of the left ventricle, and how does it define changes in left
ventricular function?
Ventricular pressure–volume loops are constructed by combining systolic and diastolic pressure
curves. The diastolic pressure curve is the relationship between diastolic pressure and diastolic
volume in the ventricle. The systolic pressure curve is the corresponding relationship between
systolic pressure and systolic volume in the ventricle. A single left ventricular cycle of
contraction, ejection, relaxation, and refilling can be visualized by combining the two curves
into a pressure-volume loop.
How is cardiac metabolism linked to O2 consumption, and how are these processes affected
by changes in cardiac work?
The goal of cardiac metabolism is to produce chemical energy (ATP) to fuel the heart function.
By doing so, the heart is able to continuously pump oxygenated blood to the rest of the body.  
Consumption of O2 by the heart depends on the amount and type of activity that the heart
performs. Under basal conditions, myocardial O2 consumption (VO2) is approximately 8 to 10
mL/minute/100 It can increase severalfold during exercise and decrease moderately in such
conditions as hypotension and hypothermia. Cardiac oxygen (O2 ) consumption is increased by:
(1) Increased afterload (increased aortic pressure), (2) Increased size of the heart, (3) Increased
contractility and (4) Increased heart rate. Therefore, Changes in O2 consumption is directly
proportional to changes in cardiac work

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