Cardiac Physiolgy & Top Facts about Heart Disease

Hello Friends !!! Watch this video to know about the Top Facts about Heart Disease before we discuss some most important cardiac physiology facts.

Hello friends. Let us discuss the factors which affect the cardiac output. So let's start with this equation and see what are the factors affecting the cardiac output. So anything which increases heart rate and increases stroke volume will increase the cardiac output. Now this stroke volume is in turn dependent on two things- one is shortening of the muscle fiber - more the shortening of the muscle fiber that means more it is contracting, it will cause increase in the stroke volume. 

And the second aspect is the size of the ventricle - more the size of the ventricle that means more muscle mass so obviously its contraction will cause increase in the stroke volume. So now let us see what things will affect these aspects. So first thing we will see is the two limbs of the autonomic nervous system. So first is a sympathetic activity. Sympathetic activity – increase in sympathetic activity leads to both increase in heart rate as well as causes increase in stroke volume by causing increase in the shortening of the muscle fibre. On the other hand there is parasympathetic activity. Parasympathetic activity decreases the heart rate but has minimal effect on the stroke volume. This should be very clear that parasympathetic activity basically supplies the S a note SA node and it affects the heart rate and not a stroke volume because there is minimal parasympathetic innervation on the muscle as such.Then next is the effect of the preload t as we are told as we are told that mainly there are four factors which are important heart rate, stroke volume preload, afterload. 

So preload also affects both heart rate and stroke volume so preload increases heart rate. This occurs by a phenomena known as Bainbridge reflex. This is basically that whenever there is an increase in the preload certain nerve fibres in the atrium are stimulated and by reflex mechanisms increase the heart rate. Plus there is also some direct stretching of the SA node which leads to increase in the heart rate. Then this preload also increases the stroke volume by increasing the shortening of the muscle fibre. This happens because of frank starling law. Now frank starling law says that force of contraction is directly proportional to the initial length of the muscle fibre so whenever preload increases what happens that it stretches the muscle fiber that is increases the initial length of the muscle fibre causing increase in the shortening of the muscle fibre. 

So see this preload is already incorporated into this equation. Now when we think about preload we should be very clear that there are multiple factors which affect the preloaded itself. So preload is first of all affected by blood volume. So increase in the blood volume will increase the preload. Then there is the effect of gravity that means suppose we change our position from lying to standing then in that case the preload decreases. Then there is contraction of our skeletal muscles and abdominal muscles that also affect the preload. Then there is ventricular compliance. That means how stiff or how compliant our ventricles are means if it is very stiff So it will not relax and if it doesn't relax it will affect the feeling of the heart. So that ventricular compliance is another factor. Then there is atrial contraction. Because atrial contraction causes the last push. It is responsible for approximately 10% of the filling of the ventricles.So atrial contraction will also affect the preload. Then another very important factor is venous complains that is how much blood the veins accommodate. Now this depends on the diameter of the veins. So if veins have lesser diameter that means they will push the blood towards the heart so that is been as compliance. Then pushed from the heart itself that is contraction of the heart that means we can say the cardiac output also affects the preload. If heart is not contracting obviously the blood will not move. So this phenomena is known as vis a ergo – pushed from behind is vis a tergo. So if there is a push from behind there is also a pull from front. That is known as vis a fronte. So there is another factor vis a fronte which affects the preload. This is basically whenever there is increase in the size of the thoracic cavity as during inspiration so it creates a negative pressure in the thoracic cavity and this creates a pull force for the blood. So this also affects the preload. Over there there is a quite overlap of arrows but don't worry in the end we will make up clearer flowchart. For you to take it. Okay now what about afternoon. Well after load actually decreases stroke volume so it actually decreases the shortening of the muscle fibre. So it so it is at this level afterload acts and decreases the shortening of the muscle fiber. So see this is also incorporated in the equation itself because afterload is affecting the stroke volume. Now right now we have drawn just one on one arrows which are affecting these four factors reload, afternoon, heart rate and stroke volume. But there is not a prosperous also because the sympathetic activity affects the venous compliance as well. When there is increase in the sympathetic activity it causes be venoconstruction and venoconstriction will in turn lead to increase in the preload. So sympathetic activity is affecting heart rate, stroke volume, as well as the preload.Also it increases the afterload because sympathetic activity causes constriction of the arterioles which are responsible for peripheral resistance. So the sympathetic activity increases after load as well. 

Then there is something known as force frequency relationship that means increase in heart rate causes increase in the stroke volume. This is known as force frequency relationship or also known as Bowditch phenomena. So this happens because when heart rate is more it causes with each cardiac impulse there is increase in calcium inside the cardiac muscle and as you might be aware that calcium is important for contraction so this increase in calcium leads to increase in the stroke volume. So guys these are the factors which affect the cardiac output. atria via internodal atrial pathways travels via cardiac conduction pathways that is to atrio ventricular node bundle of His, its right and left branches and the Purkinje fibers. The spread of electrical activity is basically depolarization of the heart muscle. Now before going into the details let us see a bit of anatomy .SA node is located at junction of superior vena cava with the right atrium and AV node is located near the interatrial septum. SA node is connected to AV node by 3 bundle of fibers arranged from anterior to posterior that is the anterior internodal tract middle and posterior internodal tract. AV node continues as bundle of His. Tt gives off a left bundle branch and continues as right bundle branch itself. These branches and their further small branches run below the endocardium layer of heart muscle, actually heart muscle has three layers right innermost layer is endocardium, middle is myocardium outermost is epicardium. So the fibers running below the endocardium and meet Purkinje fibers. So how the electrical potential spreads throughout heart. Action potential originates at SA node, moves via atrial internodal tracts to AV node. Now since cardiac muscle cells are connected to each other by gap junctions, the potential starts spreading to other cardiac cells also, since ions can pass via gap junctions to other cells so potential spreads via the conduction pathway and also along the atrial muscle cells via gap junction. It takes only about 0.1 seconds for the activity to spread to atria. Now conduction in AV node is slow and there is a delay of about 0.1 second here. This is known as AV nodal delay. 

After this the depolarization spreads by a bundle and it's branches first to the left side of interventricular septum, at midpoint of septum it moves to right and then further spreads down the septum to apex of the heart, then it turns back and reaches atrioventricular groove. Because of this last part of heart to be depolarized is postero basal part of left ventricle. This whole process of ventricular depolarization finishes in 0.08 to 0.1 seconds. Also if we consider the layers of heart remember that these fibers run subendocardialIy so electrical activity moves from endocardium to epicardium. During all this process do not forget that heart is a syncytium because of gap junctions and electrical activity spreads to other muscle cells via gap junctions. Then you may ask that if potential can pass via muscle cells then what is the need of the conduction pathways. Well there are two things the spread is faster through this conduction pathway so it facilitates rapid depolarization of heart that is rapid spread of electrical activity. Secondly from atria t0 ventricles the activity can spread only via this conduction pathway since atrial and ventricular fibers are separated by a fibrous tissue ring. This is also important physiologically because it helps in spacing the depolarization of atria and ventricles, otherwise both of them will contract together which we don't want in heart .These fundamentals we will again consider in another video on ECG and then in arrhythmias but before finishing we will also consider abnormalities in conduction pathways and diseases which may occur. Now remember that apart from SA node each part of conduction pathway is capable of generating electrical impulse but SA node generates impulses at fastest rate. That's why it is known as PACEMAKER. Also in abnormal situations even myocardium can generate electrical impulses. Secondly also remember that one spread of action potential means one heartbeat- one contraction. Now let us discuss some abnormalities diseases may occur either due to ibnormality in generation of impulse or in conduction of impulse or both, So it is occurring at various levels. First let us see SA Node. Diseases may affect SA node leading to decreased generation of nerve impulse and may cause severe bradycardia. Second there may be conduction block from SA node to AV node and below. 

Now there are levels of this block- when there is simply slowing of conduction from atria to ventricles- it is known as incomplete heart block. Another level is when there is complete block of conduction from atria to ventricles-that means no impulse which is generating at atria is reaching the ventricles that is known as complete heart block. Now incomplete heart block also may be of different grades -the first grade in which it causes prolonged duration of conduction only but all the impulses are being conducted to ventricle- Second one there may be missed beats so like two impulses are getting transmitted to ventricles but the third one may be missed or there may be another pattern like three impulses are getting transmitted but every fourth impulse is getting missed so these are two different grades of incomplete heart block. Now if we combine this incomplete and complete heart block we can say that heart block has different grades. Only prolonged duration of conduction is known as first degree heart block, when some beats are missed in between it is known as second-degree heart block and when there is complete block of conduction from atria to ventricles it is known as third-degree heart block. Now in complete block when ventricles beat at their own slow rhythm known as Idioventricular rhythm. This may occur either due to AV node disease or a block below the node. The block occurring due to AV nodal disease is known as AV nodal block and that occurring below the node is infranodal block. In some cases rate of heart beating may be so low that it leads to decrease in blood supply to brain causing fainting attacks. This condition is known as Stokes Adams Syndrome. heart blocks can also occur due to bundle branch block where the conduction till bundle of His is normal but below the conduction is affected. Apart from this abnormalities in generation and conduction of impulses can occur if there is an abnormal focus apart from SA node which is irritable and generates action potential .

Now here since myocardium is a syncytium that potential will also spread to the heart causing extra beat. If abnormal focus is too much active and its frequency of generation of action potential is higher than SA node it will cause tachycardias- these are known as paroxysmal tachycardias and depending on the location of the focus they can be atrial ventricular or nodal tachycardias. Next there can be reentry of potential. See normally there is a particular direction in which the electrical activity travels and you see once the spread occurs it does not spread back because the muscle cells are refractory .That is during an electrical activity they do not respond to second stimulus for some time so they are refractory. Now if there is a channel established such that current flows in one direction, travels via another path, comes to original place after some time such that the cells are no longer refractory, then it will depolarize the cells again and it will keep moving in a round round circle that is known as circus movement of the electric current.