Get iOS App. Solution: Stroke volume is the amount of blood ejected by the left ventricle in one contraction. The stroke volumes for each ventricle are generally equal, both being approximately 70 mL in a healthy kg man.
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Heart rate HR also affects SV. Changes in HR alone inversely affects SV. However, SV can increase when there is an increase in HR during exercise for example when other mechanisms are activated, but when these mechanisms fail, SV cannot be maintained during an elevated HR. These mechanisms include increased venous return, venous constriction, increased atrial and ventricular inotropy and enhanced rate of ventricular relaxation.
Normal values for a resting healthy individual would be approximately mL. Consequently, the alteration of PP due to a perturbation in LV elastance can be quantified as follows: So, whether PP increases or decreases depends on the sign of.
Though not definitive, it can be shown numerically that takes negative values over the space of physiologically nominal parameter values.
Therefore, should there be any notable impact of end-diastolic volume on LV elastance, the underestimation of SV based on PP will be alleviated during an increase in end-diastolic volume, for example, during fluid therapy. In contrast, the underestimation of SV based on PP will be exacerbated during a decrease in end-diastolic volume, for example, hemorrhage. To numerically examine the results of the analysis in this section, a simulation model developed by Ursino [ 44 ] and Ursino and Magosso [ 45 , 46 ] was used to create SV and PP responses to a wide range of hypothetical volume perturbations.
The model includes a time-varying elastance model of the heart, arterial and venous vessels lumped into 12 compartments, and a nonlinear baroreflex feedback model.
In the simulation model, blood volume was varied from 3. A representative result is shown in Figure 3 , where PP has been scaled to SV so that their values at 3. First of all, the simulation result shown in Figure 3 makes sure that the change in PP underestimates that in SV.
For example, the change in SV as predicted by the change in PP in response to the added blood volume of 3. Therefore, PP must not be used as a linear predictor of SV. It is noted that the result shown in Figure 3 was obtained in the presence of realistic variability in , , and. Indeed, the baroreflex feedback responses in Figure 3 indicate that these parameters were subject to nonnegligible variability during blood volume perturbation.
In particular, decreased by large amount in response to an increase in blood volume, which was attributed to a large decrease in HR thus a large increase in. Also, TPR as well as arterial and LV elastances decreased as blood volume increased, which was anticipated. Compared with LV elastance, however, the variability in arterial elastance was significantly larger due to large changes in HR and TPR. To quantitatively examine the effect of variability in , , and on our analysis, the sensitivity of SV and PP to these parameters was computed and scrutinized see Figure 4.
Overall, the sensitivity of SV on and was very small see Figure 4 a. Also, it does not explicitly depend on as indicated by 8. Indeed, simulated SV as shown in Figure 3 was very close in value to SV predicted from 8 under constants and not shown. On the other hand, PP turned out to be largely affected by these parameters see Figure 4 b. Considering that the absolute amount of change in was much larger than that in see Figure 3 , it turned out that the effect of changes in and on PP was dominant in comparison with the effect of change in.
Now that the direction of changes in and is the same i. So, together with the observation that end-systolic pressure was consistently higher than MAP see Figure 3 , PP was overestimated based on To experimentally examine the validity of mathematical analysis conducted in this study, we analyzed a subset of - loop data collected in a previous study [ 47 ].
Data pertaining to 5 human subjects were analyzed, each of which had LV - loops associated with multiple LV volumes, electrocardiogram ECG , and central aortic BP waveform.
In each - loop, ECG was used to identify the beginning of diastole. Then, end-diastolic and end-systolic LV volumes were derived as average LV volume values during isovolumetric contraction and relaxation phases, respectively. SV was then determined by subtracting end-systolic volume from end-diastolic volume. PP was derived directly from the central aortic BP waveform. On the average, the value between SV and calibrated PP was only 0.
It is also obvious in Figure 1 that the trend of underestimation was more significant as LV volume increased especially in subjects 1, 2, 4, and 5, although in subject 5 outliers were observed due to noisy LV - loop measurement.
All in all, observations from Figure 5 are highly consistent with the mathematical analysis conducted earlier in this study Section 3. It is also worth mentioning that the experimental data indicated that i MAP and end-systolic pressure were very close to each other, and that ii the experimentally observed behaviors of arterial and LV elastances, normalized DP time instant , and MAP in response to perturbations in end-diastolic volume were also consistent with the mathematical analysis conducted in Sections 3.
Second, the trends of , and were all inversely proportional to end-diastolic volume, while MAP was proportional to end-diastolic volume. Third, comparing the amount of changes in , and , the change in dominated those in and see Figures 3 and 6 , which, as discussed in Section 3. Therefore, together with Figure 5 , Figure 6 supports the validity of our mathematical analysis see Section 3. Pulse pressure has been observed to underestimate stroke volume in recent experimental studies, but the mechanisms underlying the relation between the two have not been clearly understood.
In this study, we elucidated the mechanisms underlying the nonlinear dependence between SV and PP. In sum, the rate of change in PP decreases with end-diastolic volume, while SV depends linearly on end-diastolic volume. Therefore, PP underestimates SV. Considering that PP is frequently used as a direct surrogate of SV, this entails an important clinical implication: nonoptimal fluid therapy may result if there is no correction to PP to compensate for its nonlinear dependence on SV.
In our opinion, the analysis conducted in this study may be useful for developing methods to enable such compensation in the follow-up studies. The authors declare that there is no conflict of interests regarding the publication of this paper.
The authors appreciate Professor David A. Kass at the Johns Hopkins University for providing them with the experimental data for this study. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Karim Bendjelid. Received 13 Feb Revised 15 Apr Accepted 24 Apr Published 20 May Abstract Arterial pulse pressure has been widely used as surrogate of stroke volume, for example, in the guidance of fluid therapy.
Introduction Stroke volume SV is the volume of blood pumped out by the heart to the arterial tree. Left-Ventricular Pressure-Volume Framework We use the left ventricular LV pressure-volume loop - loop framework [ 33 ] to mathematically analyze how changes in SV and PP are related during volume perturbation. Figure 1. Left ventricular pressure-volume loop for different end-diastolic volumes. Figure 2. Table 1. Effect of arterial elastance on the responses of end-systolic pressure, PP, and SV.
Table 2. Figure 3. A representative result of SV, BP, and baroreflex responses to a wide range of perturbation in blood volume 3. Figure 4. You are here Home » Cardiac Output.
Top of the page. Topic Overview For the body to function properly, the heart needs to pump blood at a sufficient rate to maintain an adequate and continuous supply of oxygen and other nutrients to the brain and other vital organs. What is a normal cardiac output? When does the body need a higher cardiac output? Why is maintaining cardiac output so important? Related Information Heart Failure. Normal physiology of the cardiovascular system.
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