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0:08
Hello, I m Eric Strong from Strong Medicine, and in today s video on the cardiovascular system, I ll be discussing cardiac mechanics referring to the physical process of the myocardium contracting and relaxing with each heartbeat. The learning objectives today: To define preload, afterload, and contractility, and to describe the factors that influence each. To calculate stroke volume, ejection fraction, cardiac output, and cardiac index. And to draw the
0:38
Frank-Starling curve. The terms preload, afterload, and contractility all suffer from the same problems. First, none have a universally agreed upon definition. And second, because they are difficult to explain and to understand, the common bedside understanding of them by healthcare professionals is usually a significant oversimplification of the relevant physiologic principles. For this discussion, I m going to take a middle-of-the-road
1:06
approach that goes into more depth than this bedside understanding, but which still steers relatively clear of nuance that is not clinically relevant. While the concepts of preload, afterload, and contractility can be applied to the mechanics of either ventricle, in common usage and how I ll use the terms in this video and in the rest of the series, they will refer specifically to the left ventricle unless otherwise stated. I ll go through them one at a time. ---
1:42
Preload can be defined either as the wall tension experienced by the left ventricle just before the onset of systole - a moment known as end diastole for which the best though imperfect - surrogate is left ventricular end diastolic pressure. Or as the sarcomere length in the left ventricle at end-diastole for which the best surrogate is left ventricular end diastolic volume. Of course, LV pressure and LV volume are related
2:10
to one another, based on the compliance of the left ventricle. And here is a graph of that relationship the pressure-volume curve. If the scale of this graph seems a little off, it will make more sense when we return to the graph when discussing pressure-volume loops in the next video in the series. We see that during diastole, the relationship starts as linear, but starts to curve upwards at high volumes. In other words, compliance
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of the LV starts to rapid decline when it s extremely stretched, as there is only so much blood the LV can hold before the walls cannot stretch any further. This an important phenomenon for patients in heart failure, whose kidneys initially try to expand their blood volume to increase both LV pressure and LV volume ultimately in an attempt to increase how much blood the heart is pumping. But when the total blood
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volume reaches a critical value, the addition of more intravascular fluid by the kidneys results in an increase in LV pressure without a significant increase in LV volume, leading to symptoms of vascular congestion in the lungs. Also, if the general compliance of the LV worsens due to infiltrative diseases of the myocardium such as amyloidosis and sarcoidosis, the overall curve steepens. So for a given LV volume, the LV pressure is higher also predisposing the patient to symptoms. Compliance
3:45
of the LV is not only dependent on the compliance of the myocardium, but is also dependent on the compliance of the pericardium, which can be adversely impacted by a large pericardial effusion or by pericardial fibrosis. So, at this point, we know 2 major things which impacts preload: total blood volume and ventricular compliance including pericardial compliance. Preload is also affected by the heart rate and heart rhythm. For one thing, there is an inverse relationship between heart rate
4:16
and preload because as the heart rate increases, the duration of diastole shortens more than the duration of systole. Thus, at faster rates, an overall less proportion of time is spent in diastole. Less diastolic filling time means less blood moves from the left atrium to the left ventricle. In addition, arrhythmias in which there is no atrial kick, such as atrial fibrillation, will necessarily also result in less left
4:45
ventricular filling during diastole. So in summary, preload is affected by the total blood volume, the heart rate and rhythm, ventricular compliance which includes how thick the wall is the thicker the wall, the less compliant. It also includes this more nebulous category of relaxation properties of the myocardium rarely called lusitropy, which can be impacted by things like ischemia. Preload is affected by pericardial compliance.
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And last, although I haven t mentioned it yet, it can also be affected by intrathoracic pressure. For example, in the presence of positive pressure ventilation, in which you can think of the air being pushed into the lungs by a ventilator rather than the lungs sucking in air from the room; that additional pressure decreases the pressure gradient driving blood back from the systemic circulation reducing preload. ---
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The most general definition of afterload is the force opposing ventricular contraction during systole that is, the mechanical load that the left ventricle must eject blood against, sometimes defined as the wall stress or wall tension during systole framing which allows for nice a parallel with preload as being the wall stress or wall tension at end-diastole. Afterload is often used interchangeably with blood pressure or vascular resistance, but
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this is a significant oversimplification. To see one way in which this is an oversimplification, we need to review the Law of Laplace. The Law of Laplace, formulated long before we knew anything about cardiovascular physiology, concerns thick-walled, fluid or air containing spheres, which in this case, will be an extremely rough approximation of the shape of the left ventricle. If we cut the sphere in half, we can see the wall and the interior cavity.
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The tensile stress experienced by the wall is very dependent on the pressure. It s usually assumed or simplified that the only relevant pressure is the intraventricular pressure that is the pressure within the ventricular cavity which is determined mostly by systemic vascular resistance itself determined largely but not completely by arterial constriction vs dilation which I ll talk more about in a future video. The intraventricular pressure
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is also determined by arterial compliance - that is, how much the aorta and large arteries momentarily distend during systole to accommodate the sudden ejection of blood before recoiling during diastole. The less compliant the arteries, for example due to calcifications and atherosclerosis, the higher the afterload will be. However, instead of the intraventricular pressure, the most relevant pressure when discussing
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afterload is more precisely the transmural pressure, which is the difference between the intraventricular pressure pushing outward and the intrathoracic pressure pushing inward. Under normal circumstances, the intrathoracic pressure is both small enough to be ignored and usually negative due to the mechanics of respiration, but as we did when discussing preload, you can imagine a patient on positive pressure ventilation, in which that positive
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intrathoracic pressure is transmitted to the heart, squeezing it a little from the outside, reducing the overall stress felt by the wall. The law of Laplace states that the wall stress equals the transmural pressure times the radius of the entire sphere, divided by 2 times the width of the wall. In other words, in circumstances where intrathoracic pressure can be ignored, afterload is proportional to the left ventricular pressure and to the left ventricular radius
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again, using the extreme approximation of the LV being spherical. Although we are talking about this in the context of afterload, the Law of Laplace can be applied to preload as well particularly if we define preload based on wall tension rather than sarcomere length. Conflating afterload with vascular resistance is also an overcomplication because left ventricular pressure is also dependent on LV outflow tract resistance. This is usually low enough to
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be ignored, but in a patient with pathologic, severe narrowing of the aortic valve a condition known as aortic stenosis or in a patient with a genetic condition called hypertrophic obstructive cardiomyopathy, this additional resistance can be significant. --- off screen In summary, the most clinically relevant influences on afterload: Afterload is increased by increased vascular resistance such as hypertension and a class of medications called vasopressors;
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by outflow tract obstruction such as aortic stenosis and hypertrophic obstructive cardiomyopathy; by increased LV chamber size and volume in other words, increased preload. And by decreased arterial compliance. Afterload is decreased by decreased vascular resistance, decreased LV chamber size such as in a patient has received diuretics a class of medications which increase the production of urine, and positive pressure ventilation. ---
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As with preload and afterload, defining contractility is tricky because how a physiologist defines it and how clinicians typically use the word at the bedside are different. I think it s most clinically helpful to consider contractility to be the intrinsic strength of myocardial contraction that is independent of both preload and afterload. Under normal conditions, it is primarily influenced by the autonomic nervous system s regulation of cytosolic calcium. --- off screen
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Contractility is increased by sympathetic activation as was mentioned when discussing excitation-contraction coupling, inotropes which is a general category of medications circularly defined as those which increase contractility. These include beta agonists like dobutamine, epinephrine, and norepinephrine, and dopamine agonists like dopamine). Increased heart rate also increases contractility via something called the Bowditch effect. This
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is the phenomenon in which cardiomyocytes have less time to move calcium out of the cytosol during diastole when diastole is shorter; thus, cytosolic calcium concentration ends up being higher than normal. Contractility is decreased by parasympathetic activation, beta blockers and calcium channel blockers, and pathologic states which interfere with either calcium handling by the cell and/or ATP generation, which includes ischemia and
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infarction, inflammation of the myocardium, severe acid-base derangements, and hypothermia among many other things. --- So why do we care about preload, afterload, and contractility? We care because they are the determinants of stroke volume, which is the volume of blood ejected from the left ventricle during systole. Stroke volume is related to the ejection fraction, which is the percentage of blood in the left ventricle that s ejected during systole. Ejection
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fraction is clinically used as a semiquantitative surrogate for contractility and overall systolic function. These two values are calculated as such: Stroke volume equals end diastolic volume minus end systolic volume. Ejection fraction as a percentage equals stroke volume divided by end diastolic volume times 100. The normal range for ejection fraction, or EF, is most commonly stated as 55-70%, though some references include 50-55% as normal, while others classify 50-55% as borderline
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. How is the ejection fraction used in medicine? Most prominently, it distinguishes different types of heart failure: specifically heart failure with preserved ejection fraction colloquially known as diastolic heart failure, and heart failure with reduced ejection fraction colloquially known as systolic heart failure. EF guides management in heart failure, specifically being one of the criteria for initiating certain
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medications such as beta blockers and aldosterone antagonists, and for placement of an implantable cardiodefibrillator. EF also guides the timing of valve replacement in valvular heart disease. Related to management questions, it aids in prognostication in a variety of diseases, including heart failure and post-myocardial infarction. Another a less common, but nevertheless important role of EF is monitoring for chemotherapy-related cardiotoxicity. However, there s a big asterisk when it comes
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to using the EF in these situations that I ll come back to when discussing Frank Starling in a few minutes. There are many different ways to measure a person s ejection fraction. The most common is echocardiography, which is another name for an ultrasound of the heart, and which is colloquially referred to as an echo. With echo alone, there are multiple approaches to measuring EF, but the most conventional is the biplane method of disks. --- off screen
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In this method, two different echo views are obtained. The apical 4 chamber view, in which the ultrasound probe is placed at the apex of the heart usually near the intersection of the midclavicular line and the 5th intercostal space. This provides one 2-dimensional view of the left ventricle in systole and diastole. The ultrasound probe is then rotated 90 degrees to acquire another view of the LV in systole and diastole.
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Tracings of the LV cavity are divided into a predetermined number of section usually 20, and using the 2 different views, the LV cavity is then subdivided into a stack of ellipsoid disks at end-systole and end-diastole, whose individual volumes can be added to provide end systolic and end diastole volumes, from which ejection fraction is calculated. There are many different variations on this method, all of which need to strike a balance between
15:16
making as few assumptions about LV shape as possible, while making the image acquisition as practical as possible. In addition to assumptions about LV shape, there is some subjectivity involved in manually tracing the LV cavity, particularly when image quality is poor due to factors like obesity, or relative immobility of the patient. --- In addition to challenges with accurately measuring EF, there s also a problem with
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using it as a surrogate for overall systolic function in patients with valvular disease. For example, consider a patient whose end diastolic volume is 110 milliliters, and end systolic volume is 50 milliliters. This makes their stroke volume 60 milliliters, and their ejection fraction 60 divided by 110, or 55% - which is normal. But what if the patient has severe mitral regurgitation a condition in which their mitral valve is incompetent
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and allows the backwards movement of blood from the left ventricle to the left atrium during systole. If a third of their ejected volume moves backwards, the effective stroke volume is only 40mL. This would suggest that the conventionally calculated ejection fraction of 55%, if used as a surrogate for overall cardiac function, is an overestimate. Framed a little differently, in a patient with severe mitral regurgitation and otherwise normal
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cardiac function, we would expect a higher than normal ejection fraction as the low pressure of the left atrium significantly reduces afterload. The same general problem is present for patients with aortic regurgitation, in which significant volume of blood falls backwards from the aorta into the left ventricle during diastole. That regurgitating blood counts as part of the stroke volume, even though it doesn t immediately enter the systemic circulation. ---
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A quantifiable physiologic parameter of overall cardiac function whose measurement does not suffer from these same limitations is cardiac output. The cardiac output is the volume of blood ejected forward from the heart per unit time. It is usually reported in liters per minute, and is sometimes abbreviated Q which is a common abbreviation in physics for fluid flow. In order to correct for differences in body size so that cardiac outputs can be compared to a reference standard, we use the cardiac
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index, which is the cardiac output adjusted for estimated body surface area. Cardiac index is reported in liters per min per meter squared. Mathematically, the cardiac output is the stroke volume times the heart rate. In other words, the blood ejected from the ventricle with each contraction, times the number of contractions per minute. And cardiac index is just cardiac output divided by the body surface area. A normal cardiac index is 2.5
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to 4.0. However, physicians do not typically calculate the cardiac output and index this way in real-life clinical situations, because as we saw with measuring ejection fraction, measuring stroke volume can involve a lot of assumptions, and is practically impossible to do for patients with irregular rhythms. So instead, there are a number of interesting techniques to measure cardiac output. They fall into invasive (or traditional) vs. non-invasive
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categories. All of them have advantages and disadvantages. As a general rule, the invasive techniques are considered more accurate, while some non-invasive techniques can provide real time, continuous cardiac output monitoring. Which technique is used for a particular patient depends on the patient and the physician, but is probably most dependent on ward and institution level preferences for example, a particular cardiac care unit might only
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measure cardiac output using the Fick method, while an ICU in the same hospital may have fully transitioned to non-invasive techniques only. I ll briefly discuss the invasive techniques since these are still relatively common in the US. The historically first described technique was pretty much the standard when I was a student: the Fick method. Conceptually, the Fick method is based on the principle of conservation of mass. Specifically, the amount of oxygen
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leaving the lungs via the pulmonary veins and ultimately the amount in the systemic arteries is equal to the amount of oxygen returning from the body via the pulmonary arteries plus oxygen added from ventilation. This oxygen added via ventilation is the oxygen that is consumed by the body s tissues. The calculation for this is cardiac output times the O2 content of mixed venous blood that is, blood from the right ventricle or
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preferably pulmonary artery that s been fully mixed since the O2 content in blood returning via the IVC and SVC are not necessarily the same, plus O2 consumption equals the cardiac output times the O2 content of arterial blood. With some quick algebraic rearrangement, we get this. And O2 content of blood is approximately equal to the hemoglobin times the O2 saturation times a correction factor, which gives us the final practical form of the calculation. So to calculate cardiac output, we need to
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know the patient s hemoglobin, and their venous and arterial O2 sats all of which are easily measured at the bedside. But wait: you re probably also wondering about that O2 consumption variable. Well that s the main problem with the Fick method directly measuring O2 consumption can be done using equipment colloquially referred to as a metabolic cart, but in practice this is not common, and physicians often make educated guesses
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about O2 consumption from published nomograms, which may or may not apply well to their specific patient. Another disadvantage is the need for an invasive measurement of venous O2 sat using a central venous catheter preferably a pulmonary artery catheter which can measure true mixed venous O2. The second invasive technique is thermodilution. Thermodilution requires a pulmonary artery catheter with a thermistor at the distal end. A thermistor is a resistance thermometer,
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or a resistor whose resistance is dependent on temperature. So in another words, it can very rapidly measure changes in temperature in real time. A small amount of relatively cold saline solution of precisely known temperature and volume is injected from the proximal port of the catheter, located in the right atrium. And the thermistor records the change in temperature that it experiences as the cold fluid passes by it while diffusing and mixing with the surrounding warm blood.
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This generates a curve of change in temperature as a function of time, in which the cardiac output in inversely proportional to the area under that curve. This is done automatically by a computer there is no need for physician to do calculus at the bedside. For a patient with low cardiac output, it takes longer for that cooled blood to make it s way completely past the thermistor, resulting in a wider curve.
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Disadvantages of thermodilution include that it also requires an invasive pulmonary artery catheter, and it s not accurate in the setting of intracardiac shunts and tricuspid regurgitation. --- The Frank Starling mechanism, also known as the Frank Staling relationship, Frank-Starling Law, and when illustrated as a graph, as the Frank-Starling curve is the observation that the stroke volume is dependent on left ventricular end diastolic volume.
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At low and normal volumes, stroke volume increases with increasing volume. This is a critically important autoregulatory mechanism that accounts for things like the moment to moment changes in preload secondary to the respiratory cycle or to abrupt changes in position. It allows the stroke volume from the right and left ventricles to match each other, even if pathology is present that asymmetrically affects one ventricle more than the other. --- off screen
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In patients who experience a brief interruption in their cardiac rhythm, for example from a premature depolarization that fails to produce contraction, the subsequent unusually long ventricular diastole will result in an unusually high amount of diastolic filling which would be a problem if the stroke volume couldn t immediately increase with the next ventricular contraction. When people experience palpitations related to premature beats, it s usually not
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the actual premature depolarization that they sense, but rather the post-pause accentuation of stroke volume that leads to a single, unusually strong pulse beat. --- However, there is a limit to this mechanism. As you can see from the graph, as the LVEDV increases into the higher than normal range, the increase in stroke volume becomes less and less, until the curve flattens. Contractility plays an important role in the Frank Starling
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mechanism. In patients whose contractility is increased, for example, by activation of the sympathetic nervous system, or by administration of positive inotropic medications, this curve shifts upwards so that stroke volume is increased at any given volume, and it takes higher volumes to reach the flat part of the curve. And for patients whose contractility is decreased, for example, due to ischemia, heart failure, or metabolic derangements, the curve is shifted
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downward, the plateau is seen at lower volumes, and in some cases, stroke volume may even decrease at extreme end diastolic volumes. There have been multiple hypotheses as to the molecular basis for the Frank Starling mechanism, but they are as-of-yet unproven. The current working hypothesis is that physical stretching of the myofibrils somehow increases their sensitivity to calcium. Some of you may already be correctly speculating
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that the stroke volume end diastolic volume relationship is dependent not only on contractility, but it s also dependent on afterload as well afterload is literally defined as the total mechanical force that is opposing ventricular contraction, so naturally, higher afterload will shift this curve downward and lower afterload will shift it upward. The last point to make here is that the ejection fraction is also dependent on LVEDV. Remember
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how EF is calculated it s the stroke volume divided by the end diastolic volume. When the curve starts to flatten, it means the stroke volume is no longer increasing with increasing end diastolic volume, so EF will necessarily decrease, even if contractility and afterload remain unchanged. This fact is very frequently but inappropriately ignored when monitoring a patient s response to heart failure management. If between two
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points in time, the EF in a patient with heart failure increased 5%, does that mean that their chronic heart failure treatment is working, or is that just because the patient skipped their usual salt-laden breakfast the day of the second measurement? And for that matter, just like the effect of afterload on stroke volume, afterload affects EF too. So a patient who forgot to take their medications the morning of their echo could have their EF measured
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as lower than it normally would be, These are some of the reasons that EF should not be used as the primary metric for monitoring heart failure. --- Let me summarize. Preload can be defined as either the LV wall tension or LV sarcomere length at end-diastole. Afterload is the force opposing ventricular contraction during systole. And contractility is the intrinsic strength of myocardial contraction that is independent of both preload and afterload.
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As mentioned earlier, these are not necessarily consensus definitions, and not every physiologist and clinician uses the words in precisely the same way. With preload, afterload, and contractility, none of these 3 are directly measured in routine clinical practice. However, there are common, convenient, and imprecise bedside surrogates used. For preload, clinicians often use central venous pressure, as measured via a central
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venous catheter in the right atrium or as estimated on exam using the jugular vein. For afterload, they use systemic vascular resistance, or if being unusually imprecise, plain old systolic blood pressure. And for contractility, they use the ejection fraction. All of these surrogates, particularly EF, should be applied with caution. Despite just talking about the problems with oversimplifying these complex physiologic
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principles, let me give you an oversimplified analogy for them. Imagine a slingshot. How far the band is stretched just before letting go is analogous to preload. The mass of the rock is analogous to afterload. And the intrinsic recoil of the band, that characteristic that is independent of the degree of stretch, is analogous to contractility. How far the rock ultimately travels is sort of like the stroke volume. So the further the band is stretched
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and the more recoil it has, and the less massive the rock is, the farther the rock will travel when released. Hopefully no physiologists will throw rocks at me with that analogy. The 4 equations that you need to remember: the calculation of stroke volume, ejection fraction, cardiac output, and cardiac index. And last, the Frank-Starling curve illustrates the non-linear relationship between LVEDV and stroke volume.
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That concludes this video on cardiac mechanics. As always, if you found the video helpful, please consider sharing it with classmates and colleagues, and consider subscribing to Strong Medicine for the rest of this ongoing series on the cardiovascular system, as well as a large collection of video on other medical topics.
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