خدمة تلخيص النصوص العربية أونلاين،قم بتلخيص نصوصك بضغطة واحدة من خلال هذه الخدمة
Introduction Cardiac output, expressed in liters/minute, is the amount of blood the heart pumps in 1 minute.This is observed in isolated myocardium, but not in living organisms, where the simultaneous decrease in vascular tone (especially with the dihydropyridine derivatives) helps to maintain and even increase cardiac output.Although an excessive increase in the end-diastolic volume may increase myocardial oxygen requirements, this intervention is associated with relatively limited consequences, as compared with catecholamines Effects of calcium entry blockers on cardiac output As calcium is essential to myocardial contraction, calcium entry blockers are expected to decrease the force of contraction of the myocardium.To try to clarify the individual roles and the combined roles of these four factors in generating cardiac output, and hence to facilitate our understanding of the effects of disease processes and therapies on cardiac output, I use a simple analogy that equates cardiac output (that is, the amount of blood pumped by the heart over a period of time) with the speed of a bicycle at a particular time point .Potentially harmful effects of vasopressor agents In contrast to the beneficial effects of vasodilator drugs, the administration of strong vasopressors may decrease cardiac output by increasing afterload, even in individuals with normal cardiac function.Beneficial effects of vasodilating substances Arterial vasodilator therapy results in significant improvements in cardiac output in patients with heart failure by reducing afterload (cycling downhill).Although most clinicians should/will be able to recite the four determinants of cardiac output - heart rate, contractility, preload, and afterload - understanding of the applicability and practical relevance of each of these four components is all too often less well ingrained.The pathophysiology of sepsis involves the release of cytokines, some of which are associated with abnormal calcium handling by the cardiac myocytes [2], leading to reduced myocardial contraction.How to measure cardiac output The amount of cardiac output can be determined through a number of medical procedures, including: o Pulmonary artery catheterization, a procedure in which a catheter is inserted into a blood vessel through a central vein, such as (the femoral vein, the jugular vein in the neck, or others) to reach the right side of the heart and then advance to the pulmonary artery.Some clinical applications Myocardial depression of sepsis Sepsis is usually associated with a normal or high cardiac output; yet many studies have shown that myocardial depression can occur even early in the course of sepsis [1], so why is cardiac output not reduced?As initially demonstrated by Otto Frank and Ernest Starling, an intrinsic property of myocardial cells is that the force of their contraction depends on the length to which they are stretched: the greater the stretch (within certain limits), the greater the force of contraction.This diagnostic procedure can be used to assess the pressure required to fill the chambers of the heart on the right side, estimate cardiac output, study the condition of the heart valves, and determine the amount of resistance of the blood vessels.Effects of inodilating substances Some drugs, such as phosphodiesterase inhibitors (milrinone, enoximone) and levosimendan, exert some inotropic effects in addition to vasodilating effects.Too little pedal power, or impaired contractility, will reduce cardiac output; however, too much effort will result in fatigue, sometimes leading to a complete collapse, with the need to slow down substantially or even to stop.Because of the simultaneous tachycardia and reduced vascular tone, however, afterload is reduced - and cardiac output can therefore be maintained or even increased.Interestingly, this therapeutic approach has been more successful than inotropic stimulation, and has been shown to reduce mortality rates in this patient population [6,7].
Introduction
Cardiac output, expressed in liters/minute, is the amount of blood the heart pumps in 1 minute. Cardiac output is logically equal to the product of the stroke volume and the number of beats per minute (heart rate). Easy enough, one may think, but the term cardiac in cardiac output is potentially misleading – with clinician's sometimes assuming that to interpret cardiac output they must focus on the heart. The heart is just one part of the much larger cardiovascular system, however, and the amount of blood it pumps is dependent on both cardiac and extracardiac factors.
Although most clinicians should/will be able to recite the four determinants of cardiac output – heart rate, contractility, preload, and afterload – understanding of the applicability and practical relevance of each of these four components is all too often less well ingrained. To try to clarify the individual roles and the combined roles of these four factors in generating cardiac output, and hence to facilitate our understanding of the effects of disease processes and therapies on cardiac output, I use a simple analogy that equates cardiac output (that is, the amount of blood pumped by the heart over a period of time) with the speed of a bicycle at a particular time point .
The analogy and the four determinants of cardiac output
Heart rate
The heart rate is perhaps the simplest determinant of cardiac output to visualize: the faster the heart beats, the more blood can be pumped over a particular period of time. Using our analogy, the faster the cyclist pedals, the faster the bicycle will go. But things are not quite so simple! Staying with the bicycle analogy, it is easy to imagine that if the cyclist pedals too fast for too long, he/she will get tired and be unable to maintain the rate of pedaling, so the bicycle will slow.
Contractility
Clearly, if the cyclist flexes his/her muscles a little and pushes harder on the pedals, then the bicycle will move faster. This can be equated to an increased contractility of the heart muscle, resulting in increased cardiac output. Too little pedal power, or impaired contractility, will reduce cardiac output; however, too much effort will result in fatigue, sometimes leading to a complete collapse, with the need to slow down substantially or even to stop.
Preload
Preload is the degree of myocardial distension prior to shortening. As initially demonstrated by Otto Frank and Ernest Starling, an intrinsic property of myocardial cells is that the force of their contraction depends on the length to which they are stretched: the greater the stretch (within certain limits), the greater the force of contraction. An increase in the distension of the ventricle will therefore result in an increase in the force of contraction, which will increase cardiac output. In our analogy, preload can be compared with a tailwind allowing the cyclist to move faster without any additional muscular effort.
Afterload
Afterload is the force against which the ventricles must act in order to eject blood, and is largely dependent on the arterial blood pressure and vascular tone. By cycling on a large smooth road rather than a narrow, bumpy one, or on a road with a gentle downhill slope, the bicycle's speed can increase significantly for a given degree of muscular effort. A tired cyclist is particularly sensitive to these aspects. Similarly, reducing afterload can increase cardiac output, especially in conditions where contractility is impaired.
How to measure cardiac output
The amount of cardiac output can be determined through a number of medical procedures, including:
• Pulmonary artery catheterization, a procedure in which a catheter is inserted into a blood vessel through a central vein, such as (the femoral vein, the jugular vein in the neck, or others) to reach the right side of the heart and then advance to the pulmonary artery. This diagnostic procedure can be used to assess the pressure required to fill the chambers of the heart on the right side, estimate cardiac output, study the condition of the heart valves, and determine the amount of resistance of the blood vessels.
• Echocardiogram, a moving image that uses sound wave technology to create an image of the heart and blood flow through the heart.
• Arterial pulse wave analysis, which calculates cardiac output from shock waves resulting from blood flow.
Some clinical applications
Myocardial depression of sepsis
Sepsis is usually associated with a normal or high cardiac output; yet many studies have shown that myocardial depression can occur even early in the course of sepsis [1], so why is cardiac output not reduced? The pathophysiology of sepsis involves the release of cytokines, some of which are associated with abnormal calcium handling by the cardiac myocytes [2], leading to reduced myocardial contraction. Because of the simultaneous tachycardia and reduced vascular tone, however, afterload is reduced – and cardiac output can therefore be maintained or even increased.
Deleterious effects of inotropic therapy
As the long-distance cyclist will know, prolonged strenuous exercise can lead to high tissue oxygen demands, which can later result in impaired muscle contraction and poor performance. Positive inotropic drugs act by different mechanisms to increase the contractility of the heart, and as such have been proposed for use in patients with cardiac failure to increase myocardial contractility and hence cardiac output. Indeed, in the short-term, acute phase of heart failure, inotropic drugs can be useful to increase cardiac output.
Beneficial effects of vasodilating substances
Arterial vasodilator therapy results in significant improvements in cardiac output in patients with heart failure by reducing afterload (cycling downhill). Interestingly, this therapeutic approach has been more successful than inotropic stimulation, and has been shown to reduce mortality rates in this patient population [6,7]. An obvious limitation is the decrease in arterial pressure, which may compromise organ perfusion.
Potentially harmful effects of vasopressor agents
In contrast to the beneficial effects of vasodilator drugs, the administration of strong vasopressors may decrease cardiac output by increasing afterload, even in individuals with normal cardiac function. This effect is seen, for example, with phenylephrine, which has almost pure α-adrenergic effects. Vasopressin may also decrease cardiac output by increasing vascular tone [8-10].
Effects of inodilating substances
Some drugs, such as phosphodiesterase inhibitors (milrinone, enoximone) and levosimendan, exert some inotropic effects in addition to vasodilating effects. This is analogous to pushing a bit harder on the bicycle's pedals at the same time as you pass the top of a hill and the road starts to go down again; the greater exertion may lead to fatigue, but the downhill slope helps to maintain speed. This is why these agents may increase myocardial oxygen requirements less than other inotropic drugs.
Effects of fluid administration
Fluid administration takes advantage of the Frank–Starling relationship to increase stroke volume and cardiac output. Although an excessive increase in the end-diastolic volume may increase myocardial oxygen requirements, this intervention is associated with relatively limited consequences, as compared with catecholamines
Effects of calcium entry blockers on cardiac output
As calcium is essential to myocardial contraction, calcium entry blockers are expected to decrease the force of contraction of the myocardium. This is observed in isolated myocardium, but not in living organisms, where the simultaneous decrease in vascular tone (especially with the dihydropyridine derivatives) helps to maintain and even increase cardiac output. The cyclist is tired, but the road is smoother, with a gentler upward slope!
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