Beyond committing the CICM examiners' definition to memory, no useful recommendations can be made. After trawling the literature, it became clear that Penefsky is the single most useful resource on this subject, as all the parameters which affect afterload are laid out in a logical pattern by the author.
A clear effort is made to produce some sort of conceptual union between the macroscopic factors which influence cardiovascular system performance as a whole and the microscopic factors which influence the performance of cell preparations.
Preload is a major determinant of contraction. The degree of sarcomere stretch at the very end of diastole is an important factor in determining the force of contraction, as we might recall from the Frank-Starling relationship. The more volume, the greater the force of contraction, until beyond a certain point the sarcomeres stretch becomes too. But that's the force of contraction. What about contractility , the " quality of this process" of contraction?
That changes too, in a predictable pattern. However, that is not the most interesting or exam-point-scoring element of this. Changes in contractility change the relationship between ventricular pressure and ventricular volume. And at this point we are compelled to discuss LV pressure-volume loops. For the explanation of the relationship between contractility and preload, the use of pressure-volume loops is made inevitable by some of the statements made by college examiners.
They started with something rather noncommittal like "a diagram of a pressure volume loop is very helpful when describing the ESPV" , but finished with an aggressive warning that "absence of a diagram correctly labelled and scaled was a weakness in many answers".
In short, you clearly need this diagram for your answer to score highly. When it is correctly labelled and scaled , the LV pressure-volume loop looks a bit like this:. Without preempting the contents of the entire PV loop chapter, the discussion of PV loops here will mainly focus on their use for describing contractility, and in particular its changes with preload and afterload. The specific use of the PV loop in the discussion of cardiac contractility is for the purpose of describing the change in end-systolic pressure with increasing end-diastolic volume.
This relationship, abbreviated as ESPVR, describes the maximal end-systolic pressure which can be achieved with that volume. Thus, if you were to plot the loop several times at different end-diastolic volume conditions, the end-systolic pressure-volume point would migrate northeast:. The relationship of these end-systolic pressure-volume points can be plotted as a line, which is the end-systolic pressure-volume relationship ESPVR :.
The more "contractile" the ventricle, the greater the change in pressure from a given level of preload. A reader well acquainted with Deranged Physiology traditions will at this stage be wondering when the author will try to support this theory by dredging up the experimental results of some abominable vivisection.
So, here is a recording of pressure-volume loops at different ventricular volumes from Kass et al , who captured these data from dog ventricles. One set demonstrates the effects of autonomic blockade with hexamethonium chloride , and the other demonstrates the effects of dobutamine.
A multitude of other methods is made possible by the lack of agreed-upon definition. This segues nicely into Specifically, in this setting, it is the maximum rate of change in left ventricular pressure during isovolumetric contraction:. This is not bad, as far as measures of contractility go. A more "contractile" ventricle should contract better harder, faster, stronger and this parameter will reflect that in a shorter isovolumetric contraction, or a higher pressure achieved over the same timeframe.
Ditto, the feeble useless ventricle will take longer to achieve a lower pressure, so it goes:. Obviously, contractility is not that simple, and this parameter has its drawbacks.
Borrowing from Mason :. It is far from perfect, and probably the kindest thing that can be said about it is that it "changes in max. In their answer to Question 4 from the second paper of , the examiners mentioned that this parameter is preload dependant and afterload independent. Where does this assertion come from? Try out PMC Labs and tell us what you think. Learn More. Cardiac output is the amount of blood the heart pumps in 1 minute, and it is dependent on the heart rate, contractility, preload, and afterload.
Understanding of the applicability and practical relevance of each of these four components is important when interpreting cardiac output values. In the present article, we use a simple analogy comparing cardiac output with the speed of a bicycle to help appreciate better the effects of various disease processes and interventions on cardiac output and its four components. 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.
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! There is an optimal rate of pedaling: too fast and the cyclist will tire too quickly and have to slow down; too slow and the bicycle will not move fast enough to cover the required distance. Similarly, if the heart rate is too slow, usually easily identified as part of a severe bradyarrhythmia, or is too fast, then cardiac output can be impaired.
Acute supraventricular or ventricular tachycardia may also be a cause of low cardiac output, and even of cardiogenic shock. 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.
This may occur with excessive inotropic support, resulting in increased mortality rates. 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. Of course, unlike our analogy — in which the speed of the bicycle will continue to increase as the speed of the wind increases — in the heart a preload value will eventually be reached at which cardiac output will no longer increase.
Preload largely depends on the amount of ventricular filling. It should not, however, be confused with the venous return. In our analogy, the venous return is like the speed of the bicycle coming towards us.
The amount of blood returning to the heart in any period of time must be equal to the amount of blood pumped by the heart in the same period, as there is no place for storage of blood in the heart.
Venous return therefore equals cardiac output, whereas preload is only one component of cardiac output. A secondary purpose was to evaluate the effects of postural position on the cardiovascular responses to incremental exercise.
Ten male cyclists participated in this investigation. Left ventricular function was assessed throughout incremental exercise in the supine and upright positions counterbalanced using radionuclide ventriculography. SVs are also used to calculate ejection fraction , which is the portion of the blood that is pumped or ejected from the heart with each contraction. Despite the name, the ejection fraction is normally expressed as a percentage. Ejection fractions range from approximately 55—70 percent, with a mean of 58 percent.
In healthy young individuals, HR may increase to bpm or higher during exercise. SV can also increase from 70 to approximately mL due to increased strength of contraction. This would increase CO to approximately Top cardiovascular athletes can achieve even higher levels.
At their peak performance, they may increase resting CO by 7—8 times. Since the heart is a muscle, exercising it increases its efficiency.
The difference between maximum and resting CO is known as the cardiac reserve. It measures the residual capacity of the heart to pump blood. HRs vary considerably, not only with exercise and fitness levels, but also with age. Newborn resting HRs may be bpm. HR gradually decreases until young adulthood and then gradually increases again with age. Maximum HRs are normally in the range of — bpm, although there are some extreme cases in which they may reach higher levels.
As one ages, the ability to generate maximum rates decreases. So a year-old individual would be expected to hit a maximum rate of approximately , and a year-old person would achieve a HR of Bradycardia may be caused by either intrinsic factors or causes external to the heart.
While the condition may be inherited, typically it is acquired in older individuals. Intrinsic causes include abnormalities in either the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest.
Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the endocrine or autonomic nervous system. In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting syncope.
While tachycardia is defined as a HR above bpm, there is considerable variation among people. Further, the normal resting HRs of children are often above bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation.
Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery.
Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood.
Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time.
CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV.
Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately bpm, CO will rise. As HR increases from to bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV.
So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between and bpm, so CO is maintained. It is also important to note that the coronary circulation nourishes the heart during diastole so as the HR increases the ability of the coronary circulation to nourish the myocardium decreases. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age.
Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata Figure The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X. Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart.
The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia the cervical ganglia plus superior thoracic ganglia T1—T4 to both the SA and AV nodes to increase heart rate, plus additional fibers to the atrial and ventricular myocardium to increase force of contraction see section on Contractility.
The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles.
Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately bpm. At the nodes sympathetic stimulation causes the release of the neurotransmitter norepinephrine NE at the neuromuscular junction of the cardiac nerves. NE binds to the beta-1 receptors and opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.
NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. Some cardiac medications for example, beta blockers work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart. Suggest this figure comes after the first paragraph.
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