Pressure Volume Time Relation 2 PDF

Pressure volume time relation 2 Doctor explanation Key information If you have any Abbreviation questions or concerns regarding Writer\Reviser: Ra...

Pressure volume time relation 2 Doctor explanation Key information If you have any Abbreviation questions or concerns regarding Writer\Reviser: Rawan Faisal Explanation this document. Writer\Reviser: Alzahra Habeeb 219-220 notes Mnemonic Book Deleted References Reference Guyton & Hall Textbook of Medical physiology 14th Edition Chapter 9 [email protected] By the end of this session, the students are expected to be able to: 1. Describe the different phases in a work loop (pressure/volume relation) during a cardiac cycle. What is the difference between stroke volume and stroke work? Identify stroke volume and stroke work from a pressure volume loop 2.Define preload. What parameters are good estimates of preload in a normal heart? What is the effect of a change in preload (load at the heart entrance) 3.Define after load. Which parameter is a good estimate of after load in a normal heart? What is the effect of an increase or decrease in arterial pressure on the cardiac workload 4. How tension/length relationship is converted to a pressure/volume loop in the heart? What is the relation between diastolic filling rate and ventricular output (the resting length-tension curve) 5.What is the relevance of the Frank-Starling mechanism to the pump function of the heart? Define cardiac contractility. What is the difference between the Frank-Starling principle and a change in cardiac contractility 6.How does sympathetic and parasympathetic activity influence heart rate, cardiac contractility and stroke work? What happens to the heart rate if the heart does not receive neural impulses Learning objectives  Pressure volume relationship The pressure changes during Volume also changes during different phases of cardiac various phases Of the cardiac cycle cycle, when valves open compared valves are closed. These changes are represented Heart valves open or close as: pressure – volume curve Volume of the left ventricle will change The pressure will change too So when we change the volume, the pressure will change because they are connected to each other Don’t panic the curve is easy and it will be explained in detail in the next slide Pressure volume relationship The pressure –volume curve Axises on the curve : Y X- axis shows you the different left ventricular volume (ml) Y- axis shows you the different left intraventricular pressure ( mmHg). There are 2 phases of the heart: Systole : cardiac muscle contraction – represented as a green line in the curve that describes the contraction period of the left ventricle. Diastole: cardiac muscle relaxes – represented as a blue line in the curve that describes the filling ( relaxation) period of the left ventricle. X 2 1 - from 50 ml, mitral valve opens In diastolic phase which leads to rapid filling of - End systolic the ventricles so it raises from Follow to the 1 2 volume= 50 ml 50 to 120 ml ( end diastolic next slide - Intraventricular pressure) pressure = 0 - No much change in diastolic pressure it is almost 0  3 4 Pressure volume relationship If we keep filling the ventricles from 120 But if we fill it more than 150, there will be dramatic increase in the left interventricular pressure. to 150ml still there is - So if you increase the volume of the left ventricle to Y no much change in more than 150 ml, there will be a sharp increase in the 8 9 the left left interventricular pressure during the diastolic interventricular phase. pressure 7 5 6 -let’s say that the left ventricle hasn’t been -Let’s say that your end filled and the volume of blood in it is 50ml systolic pressure is 50 ml and 6 - Notice that even when the cardiac muscle you filling to 120 ml contract with less volume, the pressure - When muscle contract the start in increasing “ because muscle in case pressure rise up to 120 5 contraction now – systolic phase 7 8 X - When you fill it - If the left ventricular 9 up to 150 ml or volume goes up to - If the left ventricular more more than 150 ml, you volume exceed more - During the can see the maximum than 180 ml, you can see 1 2 3 4 systolic phase, pressure reach the the pressure start pressure my peak up to 280 or 290 dropping duo to increase to 200 mmHg if you fill the ventricles more than their capacity ,the restriction (fibrous tissue or the overlaying pericardium ) so if you exceed its capacity, even the actin and myosin will starch apart and they will fail to contract – they will fail in initiating the contraction of the muscle – do muscles is not able to contract and the pressure start to drop Pressure volume relationship So in this graph we have to understand - How much is pressure during the diastolic phase - How much is pressure during the systolic phase Y - And in between your EW ( External Work is shown) and what happens 8 9 during the normal cardiac cycle. - You can see different phases during the external work - This external work will give us our stroke volume so we will see what changes happening in external work 7 6 From EW we know - End systolic volume = 50 ml - End diastolic volume normally about = 120 ml 5 X And what changes may happen during the cardiac cycle.. In the next slide 1 2 3 4 Pressure – volume relationship it is further elaborating of the same graph the same ( EW – external work) So as I have told you ( volume and pressure ) change when in the previous the valves are open and when the valves are closed slide A – V valves open at start of filling phase The same valves close at the start of systole Semilunar valves open at start of ejection phase The same valves close at the end of ejection Pressure – volume relationship it is further elaborating of the same graph the same ( EW – So as I have told you ( volume and pressure ) change when external work) the valves are open and when the valves are closed in the previous and atriocntacrtion( contraction of the atrium ) will further slide contributes about 20 % of blood A – V valves open at start of filling phase. 1 3 2 So here are shown that at and That (50 ml which is the end atriocntacrtion opening systolic volume which ( contraction of will lead to remain in the ventricles at the atrium ) period of the end of contraction) here will further rapid filling the ( mitral valve which is contributes followed by the AV valve – about 20 % of slow filling atrioventricular valve- opens blood Now the filling reaches up to 120 ml 1 2 3 Pressure – volume relationship it is further elaborating of the same graph the same ( EW – The same valves close at the external work) in the previous start of systole slide 4 When the left ventricle contract the first thing to happen is the closure of AV valve - in the case of the left side ( mitral valve)- when the muscle start contracting the blood will find the quick escape, it tries to go back so immediately the blood strike to the valve and mitral valve closes. 5 5 Now the muscle will generate energy ( the power ) to pump this blood to overcome the pressure which is already present in the aorta to open the aortic valve which is at rest the pressure at 80 mmHg so the cardiac 4 muscle pump this blood by force to overcome the pressure of aorta So during this phase the cardiac muscle is generating energy, when mitral valve is closed and aortic valve is not opened this phase is called ( Isovolumic contraction) In 1 this phase the cardiac muscle uses maximum o2 2 3 consumption to generate the ATP which is needed to develop the strength  7 Pressure – volume relationship 8 Semilunar valves open at start of ejection phase 6 7 because of the forceful contraction pressure 6 starts rising above 80mmhg it reaches to at the about 120 mmHg because when muscle pressure of contracting up to 80 mmHg it will open 80mmHg the aortic valve but because contraction of the 5 aortic valve muscle is so forceful it exceeds the pressure opens. of 80 and reaches 120 mmHg 8 diastolic phase starts with From 120 mmHg when the the closure of the aortic pressure of the aorta start valve. 4 dropping then it further it will lead to closer of the Systolic phase starts with aortic valve. the closure of the mitral valve. 1 2 3  7 Pressure – volume relationship 8 The same valves close at the end of ejection 6 9 So closure of the aortic valve start the diastolic phase. So Aortic valve is closed but at the same time mitral valve hasn’t opened yet and this is called isovolumic relaxation. So during this ( isovolumic relaxation ) the left side of the 9 heart looks like closed chamber followed by the opining of the 5 mitral valve and again the cycle repeats -In between this, ejection works. -the external work is your stroke volume which is equal to 70 ml of your 4 blood. This 70 ml which is pumped is your external work of that cycle. So 70 ml pumped out of 120 ml and 50 ml remains 1 2 3 Pressure – volume relationship Stroke volume varies on heart’s condition and on venous return. It states that external work which is your stroke volume, depends on: 1- the condition of your heart ( How healthy your cardiac muscle itself ). 2- your venous return (how mush is the filling ) Stroke work (external work) – it is the energy converted by heart to pump blood per beat. Minute work output = work output of heart / min (CO = SV*HR) Total min workload is calculated as Total work out put of heart in one beat X heart rate = minute workout ( CO) - Don’t hesitate with terminology Minute work out = CO cardiac output External work = stoke volume  In the upcoming slide factors that affect VR ( venous return) and the sate of the cardiac muscle for the contraction will Concept of preload be explained Preload: It is the tension in the ventricles when they begin contraction Preload its your end diastolic volume which is the amount of blood present in ventricles at the end of diastolic phase which is need to be pumped out. so it is load in muscles If there is a Load, you can use term tension in the ventricles when they begin to contract. that means if there is less volume can contract by force. For example, if the wight is less like when you have luggage of 1Kg, you can easily carry it but the same luggage of 5Kg, you will find it difficult to carry it. Because this luggage wight on the muscle of your arm The same if the load or tension is less the muscle, it will contract by force because it has more energy – if you increase your load, it will affect the sate of contraction of the muscle.  Concept of preload Preload corresponds to volume / pressure at the end of diastole [Itcanincrease/decrease] It sates that preload depends upon the volume ( end diastolic volume ) home much volume it received. On the bases of the volume of the left interventricular volume , we have seen special changes We have seen up to 150ml, it can accommodate If you exceeding the volume above 150 ml, we notice there is sharp increase in the pressure Preload corresponds to volume , if you increase the volume – of blood - you increase the pressure. maximum limit between 150- 160ml depending on the person’s heart condition and the build of the cardiac muscle  Concept of preload Factors leading to increase in preload result in higher cardiac contraction If you increasing the preload which is the end diastolic volume, we can have powerful cardiac contraction but at their limits which is going to be explained in ( frank starling law ). From previous slide we knew that Cardiac muscle can take up to 150 ml , lead to powerful contraction But if you go beyond the limit, muscle can ‘t contract by force.  Cardiac condition depends upon preload and afterload Preload depends on volume ( venous return ) how much volume is there Afterload Afterload Pressure in the arteries (aorta, pulmonary arteries) against which the ventricle must contract, higher pressure results in vascular impedance. Higher pressure results in vascular resistance So when we aske what is your afterload ? It is the resistance of the vessels ( entire vasculature on the heart ) on the heart. The whole body received broad network of vasculature to receive o2. Major arteries divide into medium arteries then into arterioles then into capillaries then venules so each is filled with blood. Each time muscle contra should be strong enough to push the blood forward So this vascular resistance is on the heart It doesn’t mean that the cardiac muscle has to pump the blood but it means that the cardiac mascle has to overcome the resistance of the whole vasculature on the body to push the blood forward. ( not only the arterial system but also the venous system. about 5- 6 litter o blood is there ,so with each contraction you are not only adding blood but you’ re pushing the blood forward. So that with each forward movement, that pushing and adding of blood and forward movement should be strong enough to return to the right side of the heart and there are other factors that facilitate them like ( your powerful pump, your skeletal muscle, tone of the muscle, the valve of the veins )so all of these vasculature resist the heart so when we use this ( afterload ) we are talking about the resist the left side of the heart and the other which is resisting the pumping action of the heart ( lungs under low resistance they are only one system ) but the left side of heart who entire body vasculature there that’s why the left side of the heart is 3 times thicker than the right side of the heart ). So when you are increasing the resistance in the patient who are hypertensive, the afterload is increased And other factors that increases the afterload will have an impact on the function of the left side of the heart  Afterload Factors that result in increased afterload include high arterial vascular resistance and stenosis of semilunar valves. Not only the vascular resistance that affect the afterload Also If there is stenosis ( narrowing of the valve ) for example the aortic valve if you narrow down the opening there will be an effect. Aortic stenosis will affect the heart muscle because if you narrow down the opening and the cardiac muscle try to force the blood out and the opening is narrow this will create overpressure on the cardiac muscle so resistance is either there is a resistance of the vasculature if the entire body or narrowing down the opening which is called ( stenosis ).  here is a good video about the preload and the afterload https://youtu.be/LqOd4Sqc9Ts Hypervolemia increasing in the blood volume , over transfusion of the fluids. if the blood volume increases the preload will increase. Keep this principle in your mind ( whenever you increase the blood volume, the blood pressure will increase. How? Increase the blood volume will increases the venous return and increasing in venous return will increase the filling of the ventricles and so as your contraction sate Regurgitation Regurgitation is when the valve failed to close properly ( partial close ) which allow the backward of the blood This vasculature resistance = TPR total peripheral resistance Is indicator of your diastolic pressure Diastolic pressure : is indicator of the pressure of the vasculature. The marked things So when someone has a high diastolic pressure you are going to use drug that relaxes the vasculature , were said by the so you are going to use the vasodilator to decrease the diastolic pressure you will not use drug that doctor affect the heart rather you would prefer to use the drug which has an action on the vasculature  Length – tension and pressure – volume relation Cardiac contraction is optimal with optimal overlap of myofilaments It sates that this is your actin and myosin and there is optimal resting state and there is normal range. With actin and myosin muscle can stretch and able to contract by force. The normal range it is from 1.8 – 2.3 microns and optimum up to 2.1 microns you can have this force of contraction So if you are stretching more than 2.3 up to 3.6 the whole stretching or over contraction that increase the length or decreases the length will affect the function cardiac muscle. In over stretching , actin and myosin will starch apart and you will not be able to elicit the contraction. In over contraction, actin and myosin overlap each other , as result you will not be able to achieve the desire effect  Length – tension and pressure – volume relation Excessive increase or decrease in the overlap will decrease cardiac efficacy why is there over stretching ? Because of the volume overload , excessive filling , or regurgitation , cardiac muscle fail ( weak muscle ) so hypervolemia, regurgitation, and heart failure will lead to overstretching of the cardiac muscle.  Relation: diastolic filling rate and cardiac output 1️⃣Increasing the end diastolic volume – leads to increased preload 2️⃣Secondary effect are observed in cardiac muscle contraction Higher preload leads to lower end systolic volume and resultant higher stroke volume in normal heart Details in the next slides  Relation: diastolic filling rate and cardiac output If the end diastolic volume is increased, the preload will 1️⃣ be increased and the contraction force will lead to more stroke volume, but there is a limit. -219- This happens in athletes & during exercise (EDV increase). -End diastolic volume is 120 ml, and could increase up to 150 ml (which is its normal maximum limit). 2️⃣-from When filling ventricles with additional volume (ex. Filling it 120 ml to 150 ml)→ the force of contraction will increase. -Increasing the contraction force lead to increased ejection (stroke volume) which will decrease the ESV. -This happens in people with normal heart conditions EDV = end diastolic volume especially with athletes- Reason in next slide ESV = end systolic volume  Relation: diastolic filling rate and cardiac output Why it happens in athletes? 2️⃣ Remember in athletes: 1-Heart chambers size is increased. So, the left heart chamber can accommodate (fit) more volume of blood. 2-Vasculature resistance is decreased (low total peripheral resistance). -How the vaculature resistance is decreased? *When athletes exercise, Nitric oxide ( which is an endothelium- derived relaxing factor) is released. *Even after finishing exercise (while resting), the endothelium of the capillaries keep producing EDRF. (This Nitric oxide or EDRF is a very powerful vasodilator. So, it reduces the resistance which leads to controlled blood pressure) EDRF = endothelium-derived relaxing factor (which is NO) Relation: diastolic filling rate and cardiac output Summary: -Increasing EDV (meaning increasing amount of blood filling ventricles at the end of diastole) lead to → increase in preload (which is amount of stretching of the ventricle). -With more preload there will be increased efficacy of contraction force of the muscle So→ it will eject more blood (increase stroke volume). -Increased stroke volume means in systole more blood is pumped out, so the blood that normally remains in the ventricle after the systole ends (ESV) will be → decreased  Frank Starling mechanism The ‘intrinsic ability’ of the heart to adapt to ‘increasing volumes of incoming blood’ is called Frank Starling mechanism of heart In simple words: It is the ability of cardiac muscle when it receives a larger amount of blood from the venous return, to adapt and pump it out The greater the heart muscles stretch [in normal heart] during filling, greater is ‘force’ of contraction and ‘blood pushed’ in aorta In general, The more the ventricles are filled with blood, the more stretched they will be and the more force of contraction will be generated, but if the ventricles were filled with an amount that overstretches the muscle to the point where the actin and myosin are too far apart, the ability of the muscle to contract will be decreased, and less blood will be pushed. -219- The stretch of the right atrium stimulates the SA node as well.  Frank Starling mechanism The stretch of the right atrium stimulates the SA node as well. -As there is more venous return, the wall of right atrium stretches that further stimulates the SA node. -Stimulation of SA node result? It increases: the heart rate, the rate of discharge (blood ejection), conduction velocity, force of contraction through purkinjie fibers. Frank starling law and cardiac pump function End – diastolic volume is on X axis in figure Stroke volume [SV] is on Y axis A to B (120ml to 150 ml) Increase in EDV from A to B, increases SV from A1 to B1 -It is showing that when you increase EDV → stroke volume increases ( in the normal healthy heart). Cardiac contractility Regulation of the volume of blood pumped by the heart Cardiac contractility depend on 2 factors: 1. Intrinsic cardiac regulation in response to blood volume flowing into the heart. Meaning the heart muscle itself decides how much blood should be pumped out in response to the blood volume 2. Control of heart rate and strength by the autonomic nervous This system is the extrinsic control This is same as previous Frank starling law and Cardiac contractility Frank Starling principle deals with cardiac activity Stroke volume and / or cardiac output curve is not a Stroke volume (ml) single curve but a family of curves The curves represent normal, lower, and higher than normal cardiac outputs  Sympathetic activity and heart Sympathetic innervation for heart originates from sympathetic chain at upper thoracic segments Heart rate and cardiac contraction are variates for sympathetic system. Increase in stimulation effects heart rate and strength Sympathetic innervation to cardiac tissues is for impulse generating cells, conductive and contractile tissues  Sympathetic activity and heart -Neurotransmitter of the sympathetic system is (norepinephrine) that works on the Beta 1 receptor. -Sympathetic has 3 dominant effects: 1-Increase heart rate 2-Increase fore of contraction of cardiac muscle 3-Increase conduction velocity of impulse coming from (SA node to → AV node → RT & LT bundle branches → purkinjie fibers -Pharmacologically: Medical terminology lesson 😄 (to be easier to memorize) : When we want to achieve these effects (effects of sympathetic Tropic = affecting, changing innervation) by drugs we use the terms: Chrono = time (as heart rate is how many beats per min) 1-Chronotropic effect which is increasing the heart rate. Ino = fiber 2-Inotropic effect which is increasing the force of contraction. 2-Dromotropic effect increase the conduction velocity. Dromo = speed (denoting actin & myosin filaments which are responsible for heart contraction)  Parasympathetic stimulation and heart Parasympathetic innervation to heart is through vagus Parasympathetic supply is mainly to the conduction / nodal tissues Parasympathetic stimulation has effects on heart rate  Parasympathetic stimulation and heart -Neurotransmitter of the parasympathetic system is (Acetylcholine) that works on Muscarinic receptors. M2 for the hear Parasympathetic: Slowing the heart rate -Has only one effect: (negative chronotropic effect) by vagus nerve -No effect on conduction velocity. -No effect on force of contraction. When the parasympathetic and sympathetic are operating together. The rate generated by SA node will be 70 to 80, but if we block both system it will increase up to 100, this is an indicator that the parasympathetic has the dominant role in regulating and decreasing the blood pressure. This is not only for the heart, the parasympathetic is dominant over sympathetic through the whole body.  Parasympathetic stimulation and heart Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction. Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a rate of 20 to 40 beats/min as long as the parasympathetic stimulation continues. In addition, strong vagal stimulation can decrease the strength of heart muscle contraction by 20% to 30%. The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the power contraction of the heart occurs. This distribution explains why the effect of vagal stimulation is mainly to decrease the heart rate rather than to decrease greatly the strength of heart contraction. Nevertheless, the great decrease in heart rate, combined with a slight decrease in heart con- traction strength, can decrease ventricular pumping by 50% or more. Q1)which one of the following will Q2)what will be the effect of increase the preload parasympathetic stimulation on the A. Heart failure heart? A. Increase the heart rate B. Vasoconstriction B. Increase the force of contraction C. Hypertension C. Increase the conduction velocity Slide 19 D. Decrease the heart rate Final exam 220 1)- A 2)-D Answers: 02/19/2022 37