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Summary - MG: Circulatory Tract (WBFA040-05)
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Lectures Medicines Group: Circulatory Tract summary with images.
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MEDICINE GROUP: CIRCULATORY TRACTINTRODUCTION – THE CARDIOVASCULAR SYSTEM
ANATOMY OF THE HEART
The heart is the transport system pump, and the
delivery routes are the blood vessels. The blood
consists of water, O2/CO2, nutrients, hormones,
ions, and cells. Arteries are blood vessels away
from the heart, whereas veins go towards the
heart. Oxygenated blood goes to the organs. At
the site of the organs there are capillaries, which
are small branches from the arteries, which will
then combine together to form the vein. The pulmonary
circulation is important for the oxygenation of the blood.
The left ventricle pumps the blood via the aorta into the
body, whereas the right ventricle pumps the blood via the
pulmonary arteries (deoxygenated) towards the lungs.
HEART RHYTHM – MECHANICAL EVENTS
The diastole is the phase during which the heart
relaxes and fills again with blood. The systole is the
phase during which the heart’s atria/ventricles
contract. The heart rhythm consists of 5 steps:
1. Late diastole: both sets of chambers are
relaxed and ventricles fill passively
2. Atrial systole: atrial contraction forces a
small amount of additional blood into
ventricles
3. Isovolumetric ventricular contraction: first
phase of ventricular contraction pushes AV valves closed but does not create
enough pressure to open semilunar valves. In this phase the volume remains the
same
4. Ventricular ejection: as ventricular pressure rises
and exceeds pressure in the arteries, the semilunar
valves open and blood is ejected
5. Isovolumetric ventricular relaxation: as ventricles
relax, pressure in ventricles falls, blood flows back
into cups of semilunar valves and snaps them closed
The pressure in the left ventricle can be set out against the
volume in the left ventricle. This causes the following figure.
Point A is phase 1 in which there is diastole and there is an
empty, relaxed heart. The pressure increases to point D,
which is phase 4.
,HEART RHYTHM – ELECTRICAL CONDUCTION
The heart rhythm is induced by pacemaker cells, which are autorhythmic cells in in the SA
node in the right atrium. These pacemaker cells have instable membrane potential, which
causes a current from the SA node to the cardiomyocytes. The depolarization of
autorhythmic cells rapidly spreads to adjacent contractile cells through gap junction. If there
is damage to the SA node, there are other pacemaker cells like the AV node and the bundle
of His. The instability of the membrane potential is caused by sodium and the sharp increase
is caused by calcium.
The electrical conduction has the following mechanism:
1. SA node depolarizes
2. Electrical activity goes rapidly to AV node via
internodal pathways
3. Depolarization spreads more slowly across atria.
Conduction slows trough AV node
4. Depolarization moves rapidly through ventricular
conducting system to the apex of the heart
5. Depolarization wave spreads upward from the
apex
The delay in the AV node prevents that the ventricles are
contracting, while the atria are still filled with blood.
Therefore, the maximum amount of blood is pumped into
the ventricles and into the arteries.
REFRACTORY PERIOD
After an action potential initiates, the
cardiac cell is unable to initiate another
action potential for some duration of time.
This period of time is referred to as the
refractory period, which is around 250
milliseconds in duration and helps to
protect the heart.
For skeletal muscle fast-twitch fibers the
refractory period is very short compared
with the amount of time required for the
development of tension. The cardiac muscle fiber has a refractory period lasts almost as
long as the entire muscle twitch. There is no accumulation of muscle tension possible in
cardiac muscle. In stimulated skeletal muscle the stimulation is rapidly repeated causing
summation and tetanus (muscle cramp).
PHYSIOLOGY AND PATHOPHYSIOLOGY OF CARDIAC MUSCLE CELLS VS
SKELETAL MUSCLE CELLS
There are three types of muscle: cardiac muscle, skeletal muscle, and smooth muscle.
These types differ in action potential mechanism and contraction mechanism. These
mechanisms are important for target sites of medication.
Difference in action potential mechanism:
- Skeletal muscle contraction is dependent on somatic motor neurons. An action
potential goes through these neurons, and it releases Ach at the neuromuscular
, junction. The acetylcholine can
bind to nicotinic receptors
(ligand-gated ion channels), which
will become open and allow Na+ to
go into the muscle. The action
potential goes over the membrane
and DHP, which is connected to
RyR ensures that calcium is
released from the sarcoplasmic
reticulum, which causes
contraction of the muscle.
- Cardiac muscle contraction is generated by pacemaker cells. These cells differ from
the cardiac myocytes as they are able to cause an action potential by themselves.
Cells are polarized, meaning that there is an electrical voltage across the cell
membrane. In a resting cell, the membrane voltage, known as the resting membrane
potential, is usually negative. This means that the cell is more negative on the inside
compared to the outside. There are ion gradients, which are maintained by ion
channels. The sodium channel is fast, calcium channel is slow, and the potassium
channel has no change in speed.
The pacemaker cells of the
SA node spontaneously fire
80 action potential per
minute, each of which sets off
a heartbeat, resulting in an
average heartbeat of 80 bpm.
Pacemaker cells do not have a
true resting potential. The
voltage starts at about -60 mV
and spontaneously moves upward until it reaches the threshold of -40 mV. This is
due to action of so-called ‘funny’ currents present only in pacemaker cells. Funny
channels open when membrane voltage becomes lower than -40 mV and allow slow
influx of sodium. The resulting depolarization is known as pacemaker potential. At
threshold, calcium channels open, calcium ions flow into the cell further depolarizing
the membrane. This results in the rising phase of the action potential. At the peak of
depolarization, potassium channels open, calcium channel inactive, potassium ions
leave the cell, and the voltage returns to -60 mV. The original ionic gradients are
restored thanks to several ionic pumps, and the cycle starts over.
Electrical impulses from the SA node spread through the conduction system and to
contractile myocytes. These myocytes have a different set of ion channels. In
addition, their sarcoplasmic reticulum stores a large amount of calcium. They also
contain myofibrils. The myocytes have a stable resting potential of -90 mV and
depolarize only when stimulated, usually by a neighboring myocyte. When a cell is
depolarized, it has more sodium and calcium inside the cell. These positive ions leak
through the gap junctions to the adjacent cell and bring the membrane voltage of
this cell up to the threshold of -70 mV. At threshold, fast sodium channels open
creating a rapid sodium influx and a sharp rise in voltage (depolarizing). L-type, or
slow calcium channels, also open at -40 mV, causing a slow but steady influx. As the
action potential nears its peak, sodium channels close quickly, voltage-gated
, potassium channels open and these result in a small decrease in the membrane
potential (early repolarization). The calcium channels, however, remain open and
the potassium efflux is eventually balanced by the calcium influx. This keeps the
membrane potential relatively stable for about 200 msec resulting in the plateau
phase, characteristic for cardiac muscle. Calcium is crucial in coupling electrical
excitation to physical muscle contraction. The influx of calcium from the extracellular
fluid is, however, not enough to induce contraction. Instead, it triggers a much
greater calcium release from the SR, in a process known as calcium-induced
calcium release. Calcium then sets off muscle contraction by the same sliding
filament mechanism for skeletal muscle. The contraction starts about halfway
through the plateau phase and lasts till the end of this phase. As calcium channels
slowly close, potassium efflux predominates, and membrane voltage returns to the
resting membrane potential. The ionic balance around the membrane is restored.
In short:
▪ Pacemaker cells (cardiocytes) do not contract
▪ The plateau phase is the main difference between the action potential of
pacemaker cells and of contractile cells
▪ Funny sodium channels are responsible for the potential phase of the
pacemaker cells
▪ Calcium channels are responsible for the rising phase of the pacemaker actin
potential
▪ Differences between pacemaker and contractile cells: contractile cell has
sarcolemma, large intracellular calcium store, different ion cells (rapid
sodium channels) and action potential initiates at -90 mV instead of -60 mV
▪ Conduction of the action potential from one contractile cell to another occurs
via ion flow through gap junctions, thereby speeding up the initiation of an
action potential in neighboring cells.
Cell type Skeletal muscle Contractile Autorhythmic
myocardium myocardium
Membrane Stable at -70 mV Stable at -90 mV Unstable at -60 mV
potential
Rising phase of Na+ entry Na+ entry Ca2+ entry
action potential
Refractory period Generally brief Long because None
resetting of Na+
channel gates
delayed until end
of action potential
STRUCTURE
Difference in contraction mechanism:
- Skeletal muscle fibers are large, multinucleate cells
that appear striped or striated under the
microscope
- Cardiac muscle fibers are also straited, but they are
smaller, branched, and uninucleate. Cells are joined
in series by junctions called intercalated disks.
- Smooth muscle fibers are small and lack striations
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