Showing posts with label cardiac. Show all posts
Showing posts with label cardiac. Show all posts
Monday, January 25, 2010
Saturday, November 15, 2008
10.28.08 organ systems: the heart, part 4
this lecture is the fourth and last in the series about the heart and accordingly looks at some of the larger ideas related to heart contractility, analyzing the cardiac cycle mechanically and graphically. the first main section was an in depth look at the entire heart cycle, displaying all events graphically in a pressure vs. time format. the second section was a mishmash of definitions mainly centered around the pressure/tension vs. length and active vs. passive tension relationships which were described in the muscle lectures and now applied to the heart in all its glory. the third section skipped back and looked at the mechanisms for contractility, specifically what enhanced and what decreased it. the fourth section was a look at the heart cycle within the context of the pressure vs. length graph and graphically demonstrated (similar to the way economics display disturbances to the supply/demand graphs) how different factors could influence the different measures of heart output, most important being stroke volume and work.
although he started with the overview of the heart cycle i think it's better to look at the contractility mechanisms first because it's a smoother transition from the previous material. we know from previous lectures that sympathetic post-ganglionic neurons innervate the SA, AV and myocardium using catecholamine neurotransmitters and adrenergic receptors. this section describes two mechanisms by which the sympathetic neurons accomplish greater contractility and relaxation (=faster heartrate). the metabotropic beta receptors on the nodes and heart facilitate the synthesis of the second messenger cAMP, which then phosphorylates a protein kinase which performs two actions: 1) phosphorylates membrane protein / ion channel which increases permeability of Ca2+, thereby increasing intracellular levels of Ca2+ available for contraction mechanism. 2) phosphorylates phospholamban, which acts to aid the sarcoplasmic reticulum in the reuptake of Ca2+, thereby speeding up relaxation of the cardiac muscle.
the second mechanism for sympathetic stimulation of the heart is with cardiac glycosides, which work by: inhibiting the Na/K pump, which leaves more Na+ ions in the cell, which reduces the concentration gradient and therefore the action of the Ca/Na ion exchanger, which leaves more Ca2+ in the cell to catalyze contraction. on the other hand, the parasympathetic neurons have two ways of de-stimulating the myocardium -- first is via an axo-axonic synapse to the sympathetic axon, which decreases the amount of sympathetic catecholamine NT released. the more direct mechanism is by decreasing cAMP synthesis on the post synaptic side, which will block the stimulation pathways described above.
the overview of the heart cycle is looked at in more depth than the first lecture mentioned: late ventricular diastole, where the blood is passively led into the heart via incoming venous pressure (either from the vena cava's or the pulmonary vein). atrial systole, which is an extra contraction of the atrium in times of stress, duress, or exercise, and is one last extra push of blood into the ventricle before the next phase: the pressure in the ventricle has now equalled and just begun to exceed that of the incoming venous / atrial pressure, so the AV valve (bicuspid or tricuspid) closes to prevent backflow and the ventricle is now a sealed container. the ventricle now undergoes isovolumic contraction, where it is squeezing against its fixed volume of blood in order to overcome the pressure in the aorta walls. once it gets up to this pressure, the semilunar valves open up and the blood starts rushing through the aortas during isotonic contraction, where the blood volume in the ventricle is decreasing via ejection but force of contraction is relatively constant. in reality, it is more of an auxotonic contraction, because the force of contraction changes significantly by the change in length of muscle fiber, first increasing, then decreasing. at a certain point, the pressure from the blood column in the aortas exceeds that of the ventricles, and the semilunar valves close back up. the emptied ventricles are now back to being a sealed, fixed volume, and needs to release pressure isovolumically in order to restart the diastole process. it contracts until the pressure drops down to below the atriums and the AV valves open up and incoming venous blood starts passively filling the thing back up.
the next section looks at the heart cycle within the context of the active/passive tension curve for the ventricles. the idea being that during diastolic filling, the passive stretching forces of the ventricle walls are at work and thus the passive tension curve can determine the point at which the filling pressure equals the venous pressure, causing the valves to close. and during systolic ejection, the active tension curve is at work, so this provides both a view of the maximum possible contractility at a certain fiber length (if the ventricle needed to contract against a higher aortic pressure), as well as the point at the end of systole at which the maximum active force equals the aortic pressure, which closes the semilunar valves back up. displaying the heart cycle graphically can be handy in terms of displaying two key measures of cardiac output: the stroke volume and internal/external cardiac work.
we look at different ways that the heart contractility can be affected. an increase in contractility will shift the active tension curve: this is essentially saying that for a given fiber length, the myocardium has the ability to contract more strongly. this means that during systolic ejection, the ventricle can maintain higher forces for shorter fiber lengths, meaning that the point at which the aortic pressure overcomes the ventricular will come later, thereby increasing the stroke volume. increasing the preload (as in, increasing the pressure of the incoming venous blood) will lengthen the time it takes before the AV valves are shut due to backpressure, which will increase the stroke volume. increasing compliance (inverse of elasticity) shifts the passive tension curve downwards and has the same effect as the last one. increasing the afterload (the pressure in the aortas that the ventricles have to overcome) will cause the semilunar valves to close earlier (because at the higher pressure of systolic ejection, the maximum force of the ventricles that can match the aortic pressure is reached earlier, at a longer fiber length), decreasing the stroke volume.
finally, two random facts about the graphs are thrown in. auxotonic contraction was already covered above. cardiac work is split into two categories: external work, which is the stroke volume times the height of isovolumic contraction, and internal work, which is graphically estimated to be the triangle formed by the beginning portion of the active tension curve and the isovolumic relaxation.
although he started with the overview of the heart cycle i think it's better to look at the contractility mechanisms first because it's a smoother transition from the previous material. we know from previous lectures that sympathetic post-ganglionic neurons innervate the SA, AV and myocardium using catecholamine neurotransmitters and adrenergic receptors. this section describes two mechanisms by which the sympathetic neurons accomplish greater contractility and relaxation (=faster heartrate). the metabotropic beta receptors on the nodes and heart facilitate the synthesis of the second messenger cAMP, which then phosphorylates a protein kinase which performs two actions: 1) phosphorylates membrane protein / ion channel which increases permeability of Ca2+, thereby increasing intracellular levels of Ca2+ available for contraction mechanism. 2) phosphorylates phospholamban, which acts to aid the sarcoplasmic reticulum in the reuptake of Ca2+, thereby speeding up relaxation of the cardiac muscle.
the second mechanism for sympathetic stimulation of the heart is with cardiac glycosides, which work by: inhibiting the Na/K pump, which leaves more Na+ ions in the cell, which reduces the concentration gradient and therefore the action of the Ca/Na ion exchanger, which leaves more Ca2+ in the cell to catalyze contraction. on the other hand, the parasympathetic neurons have two ways of de-stimulating the myocardium -- first is via an axo-axonic synapse to the sympathetic axon, which decreases the amount of sympathetic catecholamine NT released. the more direct mechanism is by decreasing cAMP synthesis on the post synaptic side, which will block the stimulation pathways described above.
the overview of the heart cycle is looked at in more depth than the first lecture mentioned: late ventricular diastole, where the blood is passively led into the heart via incoming venous pressure (either from the vena cava's or the pulmonary vein). atrial systole, which is an extra contraction of the atrium in times of stress, duress, or exercise, and is one last extra push of blood into the ventricle before the next phase: the pressure in the ventricle has now equalled and just begun to exceed that of the incoming venous / atrial pressure, so the AV valve (bicuspid or tricuspid) closes to prevent backflow and the ventricle is now a sealed container. the ventricle now undergoes isovolumic contraction, where it is squeezing against its fixed volume of blood in order to overcome the pressure in the aorta walls. once it gets up to this pressure, the semilunar valves open up and the blood starts rushing through the aortas during isotonic contraction, where the blood volume in the ventricle is decreasing via ejection but force of contraction is relatively constant. in reality, it is more of an auxotonic contraction, because the force of contraction changes significantly by the change in length of muscle fiber, first increasing, then decreasing. at a certain point, the pressure from the blood column in the aortas exceeds that of the ventricles, and the semilunar valves close back up. the emptied ventricles are now back to being a sealed, fixed volume, and needs to release pressure isovolumically in order to restart the diastole process. it contracts until the pressure drops down to below the atriums and the AV valves open up and incoming venous blood starts passively filling the thing back up.
the next section looks at the heart cycle within the context of the active/passive tension curve for the ventricles. the idea being that during diastolic filling, the passive stretching forces of the ventricle walls are at work and thus the passive tension curve can determine the point at which the filling pressure equals the venous pressure, causing the valves to close. and during systolic ejection, the active tension curve is at work, so this provides both a view of the maximum possible contractility at a certain fiber length (if the ventricle needed to contract against a higher aortic pressure), as well as the point at the end of systole at which the maximum active force equals the aortic pressure, which closes the semilunar valves back up. displaying the heart cycle graphically can be handy in terms of displaying two key measures of cardiac output: the stroke volume and internal/external cardiac work.
we look at different ways that the heart contractility can be affected. an increase in contractility will shift the active tension curve: this is essentially saying that for a given fiber length, the myocardium has the ability to contract more strongly. this means that during systolic ejection, the ventricle can maintain higher forces for shorter fiber lengths, meaning that the point at which the aortic pressure overcomes the ventricular will come later, thereby increasing the stroke volume. increasing the preload (as in, increasing the pressure of the incoming venous blood) will lengthen the time it takes before the AV valves are shut due to backpressure, which will increase the stroke volume. increasing compliance (inverse of elasticity) shifts the passive tension curve downwards and has the same effect as the last one. increasing the afterload (the pressure in the aortas that the ventricles have to overcome) will cause the semilunar valves to close earlier (because at the higher pressure of systolic ejection, the maximum force of the ventricles that can match the aortic pressure is reached earlier, at a longer fiber length), decreasing the stroke volume.
finally, two random facts about the graphs are thrown in. auxotonic contraction was already covered above. cardiac work is split into two categories: external work, which is the stroke volume times the height of isovolumic contraction, and internal work, which is graphically estimated to be the triangle formed by the beginning portion of the active tension curve and the isovolumic relaxation.
10.24.08 organ systems: the heart, part 2
this lecture, second in the series of the heart, introduced the finer details of heart contraction and the nervous system's influence over it. the first broad section was about the general components of the action potential mechanism in the hearts. cardiac muscle is introduced as an intermediate between skeletal and smooth muscle, in that it has similarities to both (striations similar to skeletal, cell size similar to smooth). the general mechanism of cardiac muscle contraction and relaxation is then described; induced by the SA and AV nodes, which both produce differently shaped AP curves, and propagating throughout the atriums, ventricles, and purkinje fibers.
the molecular mechanism is described as well: Na+ channels initiate the AP and immediately deactivate. Ca2+ plays a crucial role in promoting a longer during AP and in the actual contraction mechanism. L-type channels have a plateau like permeability curve, representing Ca2+ ions flowing in for a long duration (~150ms), which keeps the AP depolarized for much longer (this is also aided by the decrease in outward K+ flux). inside the cell, Ca+ stimulates further release of intracellular calcium from the sarcoplasmic reticulum, which provides the Ca2+ that is mainly used in the muscle contraction. the actual contraction mechanism is nearly (or completely?) identical to skeletal muscle -- Ca2+ binds to troponin, etc. etc.
the nodes are looked at in further detail. the SA node is the sinoatrial node, which is the primary pacemaker of the heart, because its frequency of depolarization is the fastest. the AV node is a conducting pathway between the atria and ventricles, and is slower due to the relative lack of gap junctions, and this allows the delay in contraction between the atria and ventricles. in the nodes, AP's are initiated by fast T-type Ca2+ channels, which are not affected by Ca2+ blockers, have no long plateau (due to the lack of the slow L-type channels), and spontaneously, autorhythmically depolarize due to the actions of the "funny" Na+ channels, which are activated by hyperpolarization and K+ flux.
finally, we zoom out and look at the overall hierarchy of nervous control over the heart, which starts all the way up in the upper brain structures and trickles down to the autonomic nervous system via the sympathetic and parasympathetic neurons. the main differences between the sympathetic vs. parasympathetic control over the heart are elucidated. the sympathetic preganglionic neurons originate in T1-5 of the spinal cord and innervate the neurons in the autonomic ganglia. the postganglionic neurons project to the heart via the cardiac plexus, stimulating the beta1 receptors on the nodes and myocardium, using NE and E as neurotransmitters. the effect on the SA node is to increase heart rate while the effect on the AV node is to increase conductivity (decrease latency?). the sympathetic innervation also uses second messengers to activate the "funny" Na channels.
the parasympathetic nervous system effect on the heart starts with the preganglionic neurons, which route out to the heart via the cardiac plexus, whatever that is, and the post ganglionic neurons innervate the nodes (but not the myocardium). the receptors used are muscarinic receptors, with ACh as the NT and with plenty of ACh esterase in the receptor areas. the vagus nerve (the name of the parasympathetic nerve), by means of directly opening K+ channels on the SA node, using g-proteins but without any second messengers such as cAMP, thereby allows greater outflow of K+ and therefore a lower membrane potential, and therefore a harder time reaching the threshold potential, thereby reducing the heartrate.
the molecular mechanism is described as well: Na+ channels initiate the AP and immediately deactivate. Ca2+ plays a crucial role in promoting a longer during AP and in the actual contraction mechanism. L-type channels have a plateau like permeability curve, representing Ca2+ ions flowing in for a long duration (~150ms), which keeps the AP depolarized for much longer (this is also aided by the decrease in outward K+ flux). inside the cell, Ca+ stimulates further release of intracellular calcium from the sarcoplasmic reticulum, which provides the Ca2+ that is mainly used in the muscle contraction. the actual contraction mechanism is nearly (or completely?) identical to skeletal muscle -- Ca2+ binds to troponin, etc. etc.
the nodes are looked at in further detail. the SA node is the sinoatrial node, which is the primary pacemaker of the heart, because its frequency of depolarization is the fastest. the AV node is a conducting pathway between the atria and ventricles, and is slower due to the relative lack of gap junctions, and this allows the delay in contraction between the atria and ventricles. in the nodes, AP's are initiated by fast T-type Ca2+ channels, which are not affected by Ca2+ blockers, have no long plateau (due to the lack of the slow L-type channels), and spontaneously, autorhythmically depolarize due to the actions of the "funny" Na+ channels, which are activated by hyperpolarization and K+ flux.
finally, we zoom out and look at the overall hierarchy of nervous control over the heart, which starts all the way up in the upper brain structures and trickles down to the autonomic nervous system via the sympathetic and parasympathetic neurons. the main differences between the sympathetic vs. parasympathetic control over the heart are elucidated. the sympathetic preganglionic neurons originate in T1-5 of the spinal cord and innervate the neurons in the autonomic ganglia. the postganglionic neurons project to the heart via the cardiac plexus, stimulating the beta1 receptors on the nodes and myocardium, using NE and E as neurotransmitters. the effect on the SA node is to increase heart rate while the effect on the AV node is to increase conductivity (decrease latency?). the sympathetic innervation also uses second messengers to activate the "funny" Na channels.
the parasympathetic nervous system effect on the heart starts with the preganglionic neurons, which route out to the heart via the cardiac plexus, whatever that is, and the post ganglionic neurons innervate the nodes (but not the myocardium). the receptors used are muscarinic receptors, with ACh as the NT and with plenty of ACh esterase in the receptor areas. the vagus nerve (the name of the parasympathetic nerve), by means of directly opening K+ channels on the SA node, using g-proteins but without any second messengers such as cAMP, thereby allows greater outflow of K+ and therefore a lower membrane potential, and therefore a harder time reaching the threshold potential, thereby reducing the heartrate.
10.15.08 organ systems: the heart, part 1
this lecture introduces the basic layout of the heart and begins to talk about blood flow dynamics. blood flows in through the inferior and superior vena cava into the right atrium, which uses its pectinate muscles and vestigial auricle to contract and squeeze the blood through the tricuspid valve into the right ventricle. while the tricuspid is open it is stabilized by chordae tendonae, which are tendons that are attached to the papillary muscles, which contract during the valve opening in order to stabilize. when the right ventricle contracts, it goes out of the pulmonary semi-lunar valve, which leads to the pulmonary vein, which leads to the lungs.
the now oxygenated blood comes back through the pulmonary artery into the left atrium, and is then let into the left ventricle via the bicuspid (or mitral) valve. once in the left ventricle, it is squeezed out through the aortic semi lunar valve into the aorta, in order to irrigate all the capillaries of the body.
systole is the expulsion of blood from the heart and diastole is the filling of the heart. the first heart sound comes from systole of the ventricles, where the atrioventricular cusps are shut closed due to the pressure from contraction. diastole is the second heart sound, which is the sound of the semilunar valves closing back up under the retrograde pressure of the column of blood in the aortas, which fill the sinuses behind the cusps of the SLV and shut it.
the coronary artery is the blood supply to the heart muscle itself. the left is split into the anterior descending and the circumflex, and the right is split into the posterior descending and the marginal. coronary bypass is when a piece of thoracic artery (for thick arteries like the anterior descending) or saphenous veins (for thin arteries like the marginal) is grafted in as a shunt to bypass any "occlusion", which is a site of blockage or damage.
the now oxygenated blood comes back through the pulmonary artery into the left atrium, and is then let into the left ventricle via the bicuspid (or mitral) valve. once in the left ventricle, it is squeezed out through the aortic semi lunar valve into the aorta, in order to irrigate all the capillaries of the body.
systole is the expulsion of blood from the heart and diastole is the filling of the heart. the first heart sound comes from systole of the ventricles, where the atrioventricular cusps are shut closed due to the pressure from contraction. diastole is the second heart sound, which is the sound of the semilunar valves closing back up under the retrograde pressure of the column of blood in the aortas, which fill the sinuses behind the cusps of the SLV and shut it.
the coronary artery is the blood supply to the heart muscle itself. the left is split into the anterior descending and the circumflex, and the right is split into the posterior descending and the marginal. coronary bypass is when a piece of thoracic artery (for thick arteries like the anterior descending) or saphenous veins (for thin arteries like the marginal) is grafted in as a shunt to bypass any "occlusion", which is a site of blockage or damage.
Subscribe to:
Posts (Atom)