 Coronary circulation supplies nutrition to heart and normal coronary circulation is approximately 5% of cardiac output. That means it comes to around 225 ml per minute. Now this coronary circulation will increase depending on the demands of the heart. So whenever oxygen requirement increases the coronary circulation can increase up to 3 to 4 times. So that much increase in coronary circulation can occur. However there are certain special characteristics of coronary circulation which we should be aware of because these are important in the various disease processes. So we will be dealing with different characteristics that first of all coronary arteries are end arteries and there is high capillary density in the cardiac muscle. We will see each of them one by one. There is presence of physiological shunting. Then what is the innervation of the heart and how it is important for regulation of coronary circulation. Then flow is directly coupled to oxygen demand because it has high oxygen extraction. Then how auto regulation of coronary circulation takes place and something about phasic coronary flow that is there is difference in coronary flow during systole and diastole. So let us talk about each of these characteristics of coronary circulation one by one. So first is that the coronary arteries are end arteries meaning meaning hardly there is any anastomosis in the arteries. So you see here in this diagram are shown major coronary arteries that is the right coronary artery and then there is left coronary artery. Both of these arteries arise from the root of aorta root of aorta and then you see left coronary artery where it is supplying it is supplying the anterior part of the left ventricle and the lateral part of the left ventricle while right coronary artery is supplying the right ventricle and also this branch is growing posteriorly. So posterior part of the left ventricle also is supplied by right coronary artery in majority of people. Now I am not going to talk about the anatomical aspects of these arteries we will restrict ourselves to physiology only. So yes I was talking about that these arteries are end arteries so these major arteries you see there is hardly any anastomosis between the arteries. The end of these arteries are supplying a particular area and there is no overlap in the supply. So that means if a particular coronary artery is blocked the area which is supplied by that particular artery there will be decrease in blood flow in that particular area. But one thing we should remember here that this anastomosis is lacking mainly in the larger arteries of the coronary circulation. When we talk about the division of the arteries you see the arteries are dividing there is presence of many anastomosis when we consider the smaller branches very small branches of these arteries which are basically in size of 20 to 250 micrometers there anastomosis is present. So yes the blockage of the major artery will lead to ischemia and ultimately infarction but some salvage is there because of the collaterals present in these smaller arteries. Also if the blockage develops slowly in these larger arteries then these anastomosis in the smaller arteries actually increase and that can little bit prevent the damaging effects of this slow blockage which is occurring as in case of atherosclerosis. However remember that as the blockage enlarges that anastomosis may not be sufficient to prevent the infarction of the cardiac muscle. Coming to another important aspect as far as these arteries are considered you see we were talking about these arteries which are present on the surface the major arteries and then the branches of these arteries dip into the cardiac muscle so there is dipping and just below the endocardium there is sub endocardial arterial plexus. So there is heart chamber right so the surface of the heart is supplied by these epicardial coronary arteries then there is these intramuscular arteries and just below the endocardial region there is sub endocardial arterial plexus. Now you see the heart chambers have blood but the oxygen which is present in this blood is not sufficient to supply the all layers of the heart instead the endocardial region which is the innermost lining see there is endocardium myocardium and there is epicardium so epicardium is the surface and here blood is present so this blood is capable of supplying oxygen only to a very thin layer of the endocardium rest area for that coronary arteries are important. Now why I am talking about this epicardial and sub endocardial arterial plexus because you see when there is contraction of the heart there will be compression right the muscles will contract and this sub endocardial arterial plexus will get compressed because it is present within the muscle just below the endocardium so it will get compressed and that will decrease the blood supply of the heart especially when the heart is contracting that is during the systole. We will talk about this concept in detail later on little bit more. Coming to the next characteristic that this cardiac muscle has high capillary density you see if we compare the capillaries in skeletal muscle versus that of the cardiac muscle what we are seeing here that say suppose that this is a schematic diagram showing these larger circles as muscle fibers and in between there is presence of these capillaries on the other hand if we see the ratio of capillary with the muscle fibers this ratio is much more in case of the cardiac muscle so number of the capillaries is increased in case of the cardiac muscle and this is important because the main mechanism for increasing the blood flow to the heart when the demand of the heart increases oxygen demand increases then it is mainly by increase in the blood flow then you might be wondering then it is same in other organs as well yes it is there but other organs also increase the oxygen extraction you see that in arteries blood is 100 saturated with oxygen but in veins how much is the saturation is it fully deoxygenated no in veins also it is 75 oxygenated hemoglobin is 75 saturated with oxygen so that is because the cells are not fully extracting the oxygen from the hemoglobin but this oxygen extraction is very high in case of the heart so for heart main mechanism to increase oxygen supply to the tissue will be by mainly by increasing blood flow only for other tissues they can increase the extraction of oxygen from hemoglobin as well so there are two mechanisms but for heart because of increased resting oxygen extraction it cannot increase it much further when the oxygen demand increases coming to third characteristic that there is presence of physiological shunting that means all the coronary circulation after supplying to the heart it doesn't get oxygenated by passing via the lung cell see it is venous blood right it should pass via the lungs there should be oxygenation and then it should go to the left side of the heart but if we see the distribution you see here there is coronary arteries arterioles capillaries veins and yes there is coronary sinus or anterior cardiac veins which drain into the heart chamber and this coronary sinus anterior cardiac veins mainly drain to the right side of the heart so they drain into the right atrium so this blood is going to enter into the right ventricle and then pass via the pulmonary circulation to the lungs and then enter into the left atrium but there is other pathways also you see this coronary artery directly drains into the heart chambers some of the arteries directly drain into the heart chambers by means of arterioluminal vessels and also there is another pathway arteriosinocidal vessels which also drain into heart chambers directly and this is not limited to right side of the heart some of them drain into the left side as well both into the left atrium and left ventricle as well so what will happen that that particular blood is not getting oxygenated in turn it is mixing with the oxygenated blood which is present in the left atrium and it is decreasing the oxygenation of the hemoglobin so that is known as physiological shemping coming to the innovation of coronary arteries coronary arteries are innovated both by sympathetic and parasympathetic nerves where sympathetic nerves release epinephrine and norepinephrine and parasympathetic nerves release acetylcholine now this norepinephrine which is released from sympathetic nerves acts on alpha receptors and is responsible for causing vasoconstriction on the other hand parasympathetic supply causing increase in acetylcholine release causes vasodilation so that is the direct effect of activation of sympathetic and parasympathetic nerves however this doesn't happen in heart this is not the effect which takes place in heart actually with increase in sympathetic nerve action there is vasodilation why is it so that is because of the indirect effects when there is increase in sympathetic stimulation direct effects causes vasoconstriction because of the action of norepinephrine on alpha receptors but this sympathetic stimulation also increases cardiac activity because of the action of epinephrine on beta receptors where it will cause increase in the heart rate and increase in the contractility so this in turn is going to increase the oxygen utilization and decrease local oxygen levels in the coronary circulation plus because of increased heart activity there will be increase in the production of metabolites that is there will be increase in carbon dioxide hydrogen ions adenosine potassium ions all this will increase locally and because of fall in oxygen levels and increase in these metabolites there is vasodilation so this is the indirect effect which is more potent so sympathetic stimulation directly causes vasoconstriction but physiologically this is not seen what is seen is vasodilation because of the increased heart activity similar thing happens with parasympathetic stimulation parasympathetic stimulation directly will cause vasodilation but parasympathetic stimulation will decrease heart activity causing decrease in oxygen utilization and this metabolite production will also decrease so basically major effect will be vasoconstriction so remember that the effect of sympathetic and parasympathetic stimulation mainly is because of their indirect effect rather than the direct effect coming to very important concept of phasic coronary flow that is coronary flow is different in systole versus diastole so let us see how it is different and what is the difference between left ventricle and right ventricle so in this graph you see x axis is showing time in seconds and y axis is showing coronary blood flow in ml per minute and also is shown aortic pressure in millimeter mercury now you see in systole systole this is the time this is the phase systole what is happening in left coronary artery coronary blood flow is falling it is decreasing but it is much more in diastole right why is it so see blood flow depends on perfusion pressure that is there is a gradient of pressure from aorta that is from where the coronary vessels are arising to the region where it is flowing so we are talking about left ventricle right so left coronary artery what will be the perfusion pressure see they are arising from the root of aorta so the pressure which is pushing will be the same as that of the aortic pressure that is 120 millimeter mercury and how much will be the gradient will depend on the left ventricular pressure so during systole left ventricular pressure is how much it is 120 millimeter mercury right that is the maximum pressure so you see how much is the pressure gradient it is zero millimeter mercury so zero pressure gradient is there so there is almost no blood flow during systole so this is during systole what happens in diastole in diastole the pressure in aorta will be 80 millimeter mercury and that in left ventricle it will be zero millimeter mercury yes that is the minimum pressure in the left ventricle during diastole so how much is the perfusion pressure it is 80 millimeter mercury so you compare when will the blood flow occur in the diastole because the perfusion pressure is 80 millimeter mercury however same is not the case on the right side which is supplied by right coronary artery you see in the graph flow is more in systole as compared to that of the diastole why is it so because again you see in right ventricle this right coronary artery is arising from aorta only so pushing pressure will be 120 millimeter mercury but what is the right ventricular pressure maximum right ventricular pressure during systole it is only 25 millimeter mercury okay so the perfusion pressure will be 95 millimeter mercury on the other hand in diastole how much will be the pressure aortic pressure in diastole is 80 millimeter mercury and right ventricular pressure again it is zero millimeter mercury so the perfusion pressure becomes 80 millimeter mercury so you see perfusion pressure is more in systole in the flow for right coronary artery so that is why in right coronary artery flow is more during the systole so what is the implication implication is that left coronary artery the region which is supplied by the left coronary artery it is not getting any flow during systole and it is only during diastole that this flow is reaching that musculature now when the contraction is occurring that time oxygen becomes less and the metabolites are accumulating but during systole these arteries are compressed also we have shown that diagram before that how subendocardial vessels will be compressed during systole so these are all compressed but during diastole when that compression will be released and the perfusion pressure is present in that time the flow is going to increase both because perfusion pressure is there and depending on the strength of contraction the metabolites would have accumulated which will dilate the arterios so there will be increased flow during the diastole but suppose when the heart rate increases what happens then the time of the diastole duration of the diastole decreases so there is less time available for the blood flow to occur but you see even heart rate increases and the metabolites also increase so the dilation will be more so even though there is less time available for coronary flow the dilation of the arterios will ensure that the blood flow is reaching the musculature however this will be compromised if there is some block in the vessels so during tachycardia the person becomes more prone for ischemic damage and that too especially in the subendocardial region because these are the vessels which are compressed during the systole second thing is that in case of aortic stenosis when the aortic valves are stenosed in that case left ventricle contracts much more powerfully so that it can overcome the resistance which the heart is facing right so that resistance has to be overcome that blood has to be ejected into the aorta so left ventricle contracts much more powerfully so oxygen demand is increasing much more in case of aortic stenosis so that's why aortic stenosis again makes the person more prone for ischemia again in which region subendocardial region because these vessels are compressed can you tell what will happen in aortic regurgitation aortic regurgitation is a state in which aortic valves are not closing properly so during diastole the blood is flowing back into the left ventricle so is it harmful for coronary circulation yes it will be harmful because you see during diastole this is the perfusion pressure which is being maintained so when the blood flows back into the left ventricle this diastolic pressure is going to decrease much more so that means the perfusion pressure during diastole is going to decrease so the coronary circulation during diastole is going to compromise so that will also make the person more prone for ischemia so that was about various characteristics of coronary circulation but before ending just one concept of auto regulation i want to talk about that yes we have said that there is auto regulation depending upon the oxygen requirement of the heart but suppose oxygen requirement of the heart is not increasing say suppose the heart is functioning normally but there is increase in the blood pressure so this increase in blood pressure will it increase coronary circulation yes perfusion pressure is going to increase because aortic pressure is increasing perfusion pressure is going to increase so it is going to increase the coronary circulation but that doesn't happen between 60 to 200 millimeter mercury of mean arterial pressure coronary blood flow remains constant if heart activity doesn't change and why does that happen this is because of myogenic auto regulation myogenic auto regulation so whenever there is increase in the blood pressure what happens there is increase in the stretch of the vessels okay so vessels is stretch the wall of the vessels is stretch now this wall is stretch it causes increase in calcium entry within the vessel wall and this calcium is important for contraction so as the calcium entry increases in the muscle there is muscle contraction so muscle contraction of the vessels what it is going to cause it is going to cause vasoconstriction so you see that the stretch is basically causing vasodilation right it is causing mechanical vasodilation it is stretching the wall but because of some physiological phenomena there is increase in the calcium entry actually there is mechanogated calcium channels mechanogated so they are detecting the stretch and they open when there is increase in stretch so these mechanogated calcium channels open there is increase in the calcium entry and this causes reflex vasoconstriction but remember here I am talking that heart activity is not changing so depending on the requirements of the heart it is the metabolic theory of autoregulation that is the metabolites which are causing change in the coronary circulation so that was all about the features of coronary circulation hope you got the concept thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel physiology open thank you