okay good afternoon and uh welcome to this lecture this particular lecture will be on cardiovascular physiology this module aims to provide some of the key physiological knowledge required to use Advanced cardiac monitoring in clinical practice and key topics covered in this module will include circulatory function particularly looking at pressure and flow physiology we'll be looking at otion delivery in terms of content and transport and trying to understand some of the key Concepts that affect cic output and that will be preload after load and contractility the heart is a very clever organ it modulates cardiovascular function to meet the metabolic demands and the needs of the body so that depending on the situation for example exercise or major surgery that we're interested in which require the body to produce either more or less energy in the form of ATP and to transport nutrients to and from uh the tissues this function requires two different physiological objectives to be achieved the first one is to provide an adequate profusion pressure in order to force blood into the capillaries of the organs and tissue profusion we can very simply Define as the input pressure and that's the pressure at the arterial end take away the resistance distance so pressure at the Venus end secondly we have to provide an adequate cardic output or adequate flow and this is to deliver oxygen and substrates to the tissues and that is the organs essentially the heart is a very clever organ it's a source of both pressure and flow both at the same time managing profusion both in terms of adequate pressure and adequate flow requires a frequent monitoring of arterial pressure and cardic output and ability to differentiate between the different causes of hypotension and the different causes of inadequate oxygen delivery the cardiovascular systems main priority is to maintain oxygen homeostasis so the oxygen delivery to the cells is always equal or greater to that of the demand but oxygen demand varies from time to time and the cardiovascular system has to adapt uh to these changing demands as time progresses and it regulates oxygen delivery increasing it when we're stressed decreasing it when we're more relaxed oxygen delivery or do2 is expressed as the cardic output measured in liters per minute multiplied by the oxygen content of the blood now the oxygen content of the blood is determined by the hemoglobin concentration and arterial oxygen saturations multiply by a small number 1.36 which represents the amount of oxygen dissolved or bounds rather per gram of hemoglobin this value is measured in Mills of oxygen per liter of blood and normal values for arterial oxygen concentration of blood will be around about 200 Ms per liter now if we assume a normal cardic output of approximately 5 lit per minute for a healthy adult and an oxygen content of 200 Ms per liter then we can see that oxygen delivery is round about 1,000 Ms per minute oxy delivery is frequently indexed for body surface area so we can have a meaningful comparison between different individuals in normal physiology however there is an excess of oxygen supply over demand providing a safety margin for us as organisms the manipulation of oxygen delivery is primarily through changes in our cardic output cardic output is defined as the amount of blood ejected from the left ventricle in one minute and is universally measured in um liters per minute and it's often again index a bit like do2 uh for body surface area with clinical application cardic output is the product of stroke volume and our heart rate and the stroke volume is the amount of blood that the left ventricle ejects in a single contraction and an average 70 kilom man it's around about 70 Ms per minute there are three main determinant of stroke volume and they are preload which could be thought of as ventricular filling contract ility which is the force that the heart contracts to expel that blood and afterload which is the resistance the ventrical sees when they altic valve opens consideration of preload afterload contractility allows us as doctors to manipulate the stroke volume in order to enhance oxygen delivery when this is required one key part of hemodynamic optimization is trying to match oxygen consumption to delivery through the manipulation or changing or the treatment of these different parameters in this section we'll focus on preload in terms of its importance to stroke volume and cardic output and we examine how changing preload will directly affect our cardic output and the importance of Venus return and a relatively New Concept called mean systemic filling pressure preload is defined as the tension of the myocardial fibers at the end of diast figuratively this concept it can't be measured so we often interpret it as the volume of the blood filling the left ventricle to our left ventricular end diastolic volume but it's actually related to degree of stretch exerts by this volume or exerted by this volume and ensuing cardiac simir length preload is affected by a number of factors including Venus return blood volume and our retrial pressure amongst other things and we optimize preload through giving fluid therapy and that can be either Crystal colloids or blood products as preload increases so does our stke volume and clinically our aim is to achieve optimal preload in order to create effective CTIC output the relationship between preload and stroke volume is defined by the Frank stalling curve now starling's law states the force of myocardial contraction is directly proportional to the initial fiber length and this means that when the volume of the ventricle at the end of diast is increased the tension of the mardial fibers is also increased and consequently the stroke volume Rises the effects of this could be seen by administering a fluid bolus here's a point on the lower end of the Frank Starling curve and as we give fluid so we increase our preload we stretch our myocardial fibers and stroke volume increases if we have a rise of 10% in our stroke volume then we Define that person as a fluid dis sponsor and that is they're onun the Steep part of the stalling curve however as we see at this end point here if we give too much fluid we overstretch those fibers and they no longer become efficient so stroke volume starts to decline now we can see the effect of increased preload if we look at a left ventricular pressure volume curve we measure pressure in the left ventricle and at the same time measure the volume in The ventricle as well now a normal ventricle fills in diasy and we can see here that the volume of the ventricle increases causing a relatively small increase in LV pressure and this is because the ventricle is quite compliant so that volume doesn't stretch it too much and the pressure change is minimum The ventricle then contracts and this is isovolumetric contraction so the left ventrical is squeezing against a closed aortic valve the volume is not changing so that valve hasn't opened yet but pressure is going up once pressure in The ventricle equals or is greater than the pressure in the aut the valve opens and the contents of The ventricle are expelled into the circulation and that's what we see here and then the heart relaxes once again coming back down to normal the difference between the enddiastolic volume and the end systolic volume is our stroke volume and we can see this as the width of the pressure volume curve here when we increase preload we're increasing the amount of blood that fills during diast so our end diastolic volume is greater this means that the heart then injects more blood that is present in The ventricle and stroke volume is increased and this increase in stroke volume is displayed as an increase in the width of the pressure volume Loop one of the ways that we increase our preload is by increasing Venus return and Venus return is a key component of our cardic output very simply vus return is defined by the mean systemic pressure that is the driving pressure taking blood back to the right side of the heart minus right atrial pressure which is the resistance to blood flow to the right atrium and we divide this by our resistance to Venus return mean systemic pressure is a rather unusual concept that is actually rarely discussed in cardiovascular physiology but it's key and essential because as we've seen it's the driving pressure that takes blood to the right side of the heart Meemic pressure is the pressure in the vascular system system if the heart stops and the pressure redistributes it's determined by the volume that extends all the elastic structures and the sum of all their individual compliances now in healthy individuals it's approximately 7 to 8 millimeters of mercury and it's an indicator of how full the system or the circulation is and that is it's the relationship between blood volume and the total capacity of the system so as we mentioned it's the driving pressure or input pressure for ven its return it's affected by blood volume invades the motor tone um these are the static determinants of uh MSP and blood flow distribution and Venus conductance of the dynamic determinant so mean systemic filling pressure or mean stemach pressure will increase if there's an increase in blood volume or a decrease in Venus compliance and hence assuming that right atrial pressure remains unchanged then the Venus return will be improved conversely mean systemic pressure will decrease if blood volume is decreased such as in Hemorrhage for example or if Venus compliance is increased through the use of various drugs and these situations will both lead to decrease in Venus return Venus return is important because essentially it is the cardic output the heart can only eject what's return to it so mean systemic pressure is a driving pressure for V return returning blood to the right atrium and hence the right atrial pressure or Central Venus pressure is the resistance to this flow it's not a measure of how full we are what the heart does is to regulate right atrial pressure which in turn Alters of in return which in turn Alters of ventricular filling and therefore a cardic output the two most commonly used measures of or methods of measuring preload are the direct measurements of central Venus pressure and Pulmonary AR pressure through catheter based techniques for many years these have been the main stay of determining fluid States for patients and individuals particularly in those who are critically unwell however the assumptions that these Methods made are ultimately flawed and these measurements do not provide an accurate measurement of fluid status Central Venus pressure or CVP is a measurement of pressure in the venne Cava close to the rise Atrium it's been typically used by clins in the assessment of intravascular volume for many many years and the assumption is that your right atrial pressure is equal to your right ventricular preload which in terms relates to your left ventricular preload also and hence Therefore your position on the staring calf the assumption that CVP equates the left ventricular end of dioic volume is however Incorrect and this is because the Assumption ignores the impact of vasomotor tone left ventricular compliance right ventricular compliance and ventricular geometry amongst other things in addition as we've discussed previously it's not right atrial pressure that is a measure of Venus return or filling this is the resistance to flow coming back to the heart it's the pressure gradient between mean systemic pressure and the right atrium that determines V return and hence our cardic output if we move on to the measurements of pul pressure then as a means to assess volume status it has the same issues as CVP and if not entirely worse measurement of a pul arter occlusion pressure requires the insertion of a pul artery catheter which is wedged into a tapering branch of one of the pulmonary arteries it can be difficult to measure as the tip must be placed exactly in West zones 3 essentially in using this measurement or this method to estimate blood volume status the underlying assumption is that pulmonary artery wedge pressure estimates or left ventricular enddiastolic pressure and hens of volume and this assumption is ultimately flawed but even assuming that's correct in normal physiology there are a number of situations where this relationship is disrupted such as in mitro stenosis uh left ventricular failure atic regurge and palmary veenus obstruction amongst others we make a number of assumptions when using pulmonary artery collusion pressure and not just that pulmonary artery wedge pressure estimates left ventricular and diastolic pressure and hence our volume we first assume that pul artery cusion pressure is approximate to pul Venus pressure and then what we do is assume this is approximate to left atrial pressure which in turn is proportional to left ventricular and diastolic pressure which in turn is then proportional to left ventricular and diastolic volume this is a significant number of assumptions to make however the most inaccurate assumption is that left ventricular end diastolic pressure equates to left ventricular end diastolic volume and the assumption that left ventricular endic pressure press is proportional to its volume is a rather dangerous one to make because the normal left ventricular endic or ventricular pressure volume curve is curvy linear in addition the relationship changes depending on ventricular compliance for the same pulm artery collusion pressure if the left ventricle has a low compliance compared to a normal ventricle then the volume in the poorly compliant ventricle is reduced and hence the filling status is overestimated conversely for the same pul artery occlusion pressure if the left ventricle has a higher compliance then the volume in the compliant ventricle is larger and hence the filling status is underestimated so once again this parameter doesn't help us decide filling status nor does it help us decide if that subject is going to be fluid responsive newer methods of determining a subject is fluid responsive are now being used in clinical practice with the two most commonly used variables being stroke volume variation and pulse pressure variation and these rely on the changes in Venus return and afterload due to mechanical ventilation which cause stroke volume and pulse pressure to change over this measured cycle these changes can be thought of as repeated mini fluid challenges and hence can determine if patients are fluid responsive or not the second determinant of stroke volume is contractility cardiac contractility very simply can defined as the tension developed and the Vel vity of shortening of mardial fibers at any given preload it resembles a unique and intrinsic ability of cardiac muscle to generate a force that is independent of any load or stretch that is applied factors that increase contractility and hence have a positive atropic effect include activation of our sympathetic nervous system circulating natural catacol and various medications that include deduction and adrenaline factors that decreased contract ility and hence have a negative entopic effect include the parasympathetic nervous Supply and various medications to depress the mardum including many anesthetic agents that we use in today's practice if we look at our normal pressure volume Loop we can see how either increasing or decreasing contractility changes these loops and hence or St volume if we increase contractility we can see The ventricle generates a higher pressure and also the rate of pressure development is also greater this leads to a decrease in the N systolic volume meaning the left ventricle has ejected more blood and the stroke volume is higher because there is less blood in The ventricle at the end of syy The ventricle fills to a slightly smaller end dioic volume but overall stroke volume which is the width of the curve is increased conversely if contractility is decreased The ventricle generates a lower pressure ejecting less blood and hence the volume at the end of contraction so our end systolic volume is lower and the stroke volume has decreased changes in contractility can also be demonstrated on the Frank Starling curve an increase in contractility shifts the curve up demonstrating that increase in contractility improves stroke volume the curve that demonstrates a decrease in contractility is shifted down laterally and therefore for any given left ventricular end diastolic pressure stroke volume drops with decreased contractility and increases with improved contractility once again going back to our end our pressure volume curves one of the accepted measurements of contractility is the slope of the end systolic pressure volume relationship the maximal pressure that can be developed by The ventricle at any given left ventricular indolic volume is defined by the N systolic pressure volume relationship if we draw repeated curves uh or repeated pressure volume curves rather for the same ventricle where contractility and afterload remain a constant however only preload changes then it's a line that connects the points at the end of syy and is called the enolic pressure volume relationship the gradient of the espvr represents contractility and is called n systolic alence essentially espvr becomes steeper and moves to the left as contractility increases and it becomes flatter and moves to the right as contractility decreases the alternative measure of contractility is the maximum change in pressure over time of the left ventricular pressure during contraction also known as DP DT that is Delta pressure DP divided by Delta time DT in clinical practice the maximal dpdt of the systolic slope of the arterial pressure wave form in a conduit artery so such as the radius can be used as an indicator or measure of contractility and this correlates with enolic relance the steeper the slope the quicker the rise in pressure over time and hence the greater the dpdt and hence the stronger the contractility the shallower the slope or slower the rise of dpdt the weaker the contractility so here we have arterial form with a high dpdt so very quick pressure change over time which represents our good contraction compared to one with a low dpdt which represents poor contractility so the final determinance of stroke volume is after load and when understanding how the heart interacts with blood vessels to generate flow it's essential to understand the arterial load that is the essentially the opposition and that must be overcome by The ventricle to eject blood into the aorta arterial load represents all the non-cardiac factors that resist blood flow and therefore we can think of it as a net measurement of our afterload afterload is increased by peripherical vascular resistance by higher Lance of our major blood vessels ventricular dilation and an increase in ventricular pressure and negative inter thoracic pressure conversely it's reduced reduction in our peripheral vascular resistance good compliance of our major blood vessels and decrease ventricular pressures and increase ventricular wall thickness decreasing AO can decrease stroke volume and this can be achieved in the clinical environments through reduction in vascular resistance traditionally systemic vascular resistance has been used to characterize the arterial system and obtain a gross simplification of afterload it's calculated by Computing the difference between our mean arterial pressure and our right atrial pressure and it's divided by the cardic output and the whole equation is multiplied by 80 measured in dine seconds per cm to the minus5 with a normal value being between 800 to 1200 but once again a Like Oxygen delivery this can be indexed for body surface area we can see how changing after load affects our stroke volume here's our original pressure volume curve here if we decrease after load there is less resistance to blood being ejected from The ventricle so it needs to generate less pressure before the aortic valve opens and in addition the velocity of the cardiac muscle fiber shortening is increased leading to an increased ejection velocity more blood being ejected and hence a decreased n systolic volume this in turn leads to a greater stroke volume if after load increased however the opposite happens with the ventricle having to generate a much higher pressure to open the atic valve and it's met with greater resistance decreased muscle fiber shortening reduces ejection velocity and we ends up with an increased n systolic volume and hence a decreased stroke volume overall in terms of measuring arterial load it can be characterized into a single number which is called effective elastins and this is the ratio of the enolic pressure divided by our stroke volume we can show this by the lines seen on here on the PV Cal and essentially the higher and the steeper the line the increased the afterload the lower the line with reduced gradient the less the afterload we can see the importance and the interaction of Venus return because if we draw the Venus return curve then we're our cardiac contractility curve that is the starting curve intersects then this is the equilibrium point on our cardiac output at any one point in time so cardiac function is determined by the intersection of the Venus rer function and the cardiac function when we give a fluid bolus we increase our mean systemic pressure therefore increasing the driving pressure and hence V return and we change this equilibrium point increasing our cardic output if we lose volume then the opposite occurs so in summary cardi output is affected by preload afterload and contractility and the interaction of these variables are complex understanding the relationship of these variables and how they can be manipulated allows the Collis to alter oxygen delivery to meet the patient's needs and is key in being able to manage a patient's H Dynamics thank you