The SA (sinoatrial node) is a pacemaker that is in the right atrium of the heart. SA node control the heart rate using the electrical impulses that sends to the heart muscles and this is how the heart pumping blood out to the entire body and how the heart contract. The stages of the pathway of action potential:
1) The Action Potential is in the Sinoatrial node (SA). Action potential then travels from the SA node to the AV (atrioventricular node) by crossing to the wall of the atrium. Then the action potentials slowly pass through the AV node and it give time for the atria to contract. 3) Then it’s rapidly passes through the atrioventricular bundle that extends to the AV node to the fibrous skeleton and into the interventricular septum. 4) AV bundle is divided into two separate bundle branches (left and right bundle branches). Then the action potentials separate into two and then each action potential goes though to each bundle branches. 5) The Purkinje fibers carried the action from the bundle branches to the ventricular walls.
The ends of the Purkinje fibers allow the ventricular muscles cells to contract because the action potential is rapidly passes through the AV bundle to the end of the Purkinje and this cause a rapid conduction and its providing a very strong contraction to the ventricular muscle. The intercalated discs are a network that allows the rapid transmission of the electrical impulses and this allows the action potentials to travel to one cardiac muscle cells to the next. Sympathetic Nervous System carry the nerve impulses from the brain (medulla oblongata) to the heart and it releases hormones (that increases the heart rate).
Parasympathetic Nervous System also releases hormones that slow down the heart rate. The hormone is called acetylcholine. The neurotransmitters are involved in sympathetic nervous system are: acetylcholine (sympathetic ganglion) and norepinephrine (post-ganglionic) and for the parasympathetic nervous system are: acetylcholine (preganglionic) and norepinephrine (noradrenaline) or epinephrine (adrenaline). Acetylcholine is for membranes of cells and Epinephrine is for liver cell. There are five phases of an action potential that is produced by the cardiac muscle cells.
Phase four is the resting phase, phase zero is the depolarization phase, phase one is the early repolarization phase, phase two is the plateau phase and phase three is the repolarization phase. Phase four is the phase where the transmembrane potential is at resting state and this makes the Na+ channel and the Ca+2 channel to close. Due to the leak of K+ (in the inward rectifier channels) the mV is -90 therefore the resting state is in cardiomyocytes. Phase zero is where the depolarization phase, this phase the transmembrane potential (TMP) increases above -90 mV because action potential set off the pacemaker cells and makes the TMP increases.
Na+ channels slowly opens each channels and this cause the Na+ to leak into the cells and makes the TMP increases further. The large Na+ current depolarizes the TMP to 0 mV and the Na+ channel slowly closes. Since the TMP is 0 mV therefore its greater than -40 mV, this makes the L-type Ca+2 channels open and then an inward current goes down the concentration gradient. Phase one is where the early repolarization phase. In this phase the TMP is positive and the K+ channels opens. The K+ flows outward and it returns to the TMP and makes it 0 mV.
The phase two is the plateau phase, the L-type Ca+2 channels in phase zero are still open in phase two. An inward current is flowing K+ in the concentration gradient to the delayed rectifier K+ channels. The Ca+2 and K+ channels are electrically balanced and the mV of the TMP is just below 0 throughout phase two. Phase three is the repolarization, this phase the Ca+2 channels is becoming inactive. Then the TMP is back to -90 mV because of the outflow of the K+ and the inward flow of Ca+2 to prepare for the new cycle of the depolarization.
By returning the Na+ and Ca+2 ions back to the extracellular environment the normal TMP ionic concentration gradient are stored and the K+ channels are remained open. In this stages the Na+-Ca+2 exchange, Na+- K+-ATPase and the Ca+2-ATPase are involved for the pumping of ions. The difference between the action potential produced by the cardiac myocyte and the action potential produced by the cardiac pacemaker cell, is the action potential that produced by the cardiac myocytes are called the “fast response” because of the fast depolarization and it can found throughout the heart except of the pacemaker.
Also the “fast response” only use calcium in certain duration of the action potential. On the other hand, the action potential produced by the cardiac pacemaker cells are called the “slow response” since the slow rate of the depolarization and this can be found in the SA and the atrioventricular node in the heart. Also the “slow response” uses the calcium to the initial depolarization of the action potential. The ultimate effect of the action potential generated in the cardiac muscle cell is that the electric impulses are longer and involuntary and the contraction are much longer.
For the supine and the two minute positions in table one, the heart rate of the participant while standing up is increasing because of the gravitational stress. Standing is automatically increases the BMP of the heart since the heart need to work harder because of the gravity and the heart need to beat faster in order to bring the blood back to the heart from the body. Standing can cause the gravitation stress since the gravity is pulling the blood in the body downward. The gravitation stress also reduces the amount blood in the brain and the upper body so that they have a constant supply of oxygen that is running in the body.
For the fifteen seconds position in table one, the heart rate of the participant while lying down is decreasing because lying down counterpoise the gravity therefore the heart doesn’t have to work harder compare when the person is standing up. For the thirty seconds position in table one, the heart rate of the participant is increasing because of the gravitational stress and the participant is standing up after lying down. In table two, supine’s P-wave is the atrial depolarization (this causes by spreading the action potential to atrial cardiac muscle from the SA node).
The QRS Complex (large collection of voltage cause a large curve). The T-wave (repolarization as the action potential cut off in the ventricles. In supine and one minute, the event’s amplitude is low because the participant is standing up. Fifteen seconds, the event’s amplitude are all the same and it increases because this is the time when the participant is lying down on the yoga mat. Thirty seconds, the event’s amplitude are the same and it decreases compare to the fifteen seconds because this the time when the participant is standing up from lying down on the yoga mat.
The atrial contraction occurs at the P-wave; in supine it occurs in -0. 018mV at 22. 25s. In fifteen it occurs in 41. 9mV at 74. 96s. In thirty seconds it occurs in 27. 2mV at 89. 79s. In one minute it occurs in 0. 203mV at 110. 03s. The ventricular contraction occurs at the QRS Complex; in supine it occurs in 0. 116mV at 22. 36s, fifteen seconds it occurs in 41. 9mV at 75. 2s, thirty seconds it occurs in 27. 2mV at 89. 96s and one minute 0. 524mV at 110. 11s. The S1; occurs at 22. 38s- 22. 42s and S2 occurs at 22. 64s-22. 70s in supine, occurs at 75. s-75. 08s and S2 occurs at 75. 18s-75. 21 in fifteen secs, occurs at 89. 98s-89. 90s and S2 occurs at 90. 10s-90. 13s in thirty secs and S1 occurs at 110. 13s-110. 16s and S2 occurs at 110. 31s-110. 34s in one minute.
There are two possible mechanisms that can affect the change of rate of the participant from supine to the standing position. The two mechanisms are the cardiac-somatic coupling (during the passive coupling the parasympathetic is produce) and the cardiac-somatic uncoupling (during the active coupling the sympathetic is produce).
