Cardiac Output Curve Research Articles

Allometric scaling of the parameters characterizing venous return surface in the generalized framework of circulatory equilibrium

Study objective: In the generalized framework of circulatory equilibrium (GCE), the integrated cardiac output (CO) curve characterizes the pumping abilities of the left and right hearts, whereas the venous return (VR) surface characterizes the preloading properties of the systemic and pulmonary circuits. Equilibrium CO (= VR), left (PLA) and right (PRA) atrial pressures are predicted from the intersection between the CO curve and VR surface. In VR surface, VR is theoretically related with stressed blood volume (V), PLA and PRA as: VR =V/W − Gs × PRA − Gp × PLA, where Gs and Gp is a ratio of systemic (Cs) and pulmonary (Cp) vascular compliance to W (time constant of the systemic and pulmonary circuits), respectively. However, there was a concern whether the standard parameters can be applicable to animals with different body size including human. The objective of this study is to experimentally investigate whether an allometric scaling of the parameters (Gs, Gp, W, Cs, Cp) of the VR surface is feasible. Hypothesis: Kleiber’s law indicates that an animal's metabolic rate scales to the 3⁄4 power of the animal's body weight (BW). Based on this, we hypothesize that Cs and Cp may be proportionate to BW, W may be proportionate to BW1/4. Hence, Gs and Gp may be proportionate to BW3/4. Methodology: Seven mongrel dogs (BW 26±2.8 kg) and 4 beagles (BW 9±0.5 kg) were anesthetized, and their left and right hearts were replaced by dual mechanical pumps. While V was kept constant, by controlling the speed of the fluid pumps, VR (ml/min), PLA and PRA (mmHg) were changed variably over a wide range to obtain six sets of VR, PLA and PRA. After the change of a known amount of V (4 mL/kg), six sets of VR, PLA and PRA were obtained in a similar manner. Using 12 sets of VR, PLA and PRA, we obtained Gs, Gp, W, Cs, and Cp using regression analysis in each animal. Finally, we analyzed relations between BW and all these parameters using regression analysis over the 11 animals. Data: Gs (r2=0.73, p value for independent variable piv<0.01; p value for intercept, pi=0.57) and Gp (r2=0.81, piv<0.01, pi=0.64) were proportionate to BW3/4. Cs (r2=0.37, piv=0.027, pi=0.40) and Cp (r2=0.61, piv<0.01, pi=0.48) were proportionate to BW. However, W (r2=-0.11, piv=0.90, pi=0.17) was not associated with BW1/4. Summary of results: All parameters characterizing VR surface except for W were significantly associated with BW. W did not show a significant association with BW, potentially due to the low variations of BW. Conclusions: Allometric scaling of VR surface may be feasible and effective in future clinical application of GCE. NTT Research, Inc. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Partial Support of the Left Ventricular Assist Device Shifts the Systemic Cardiac Output Curve Upward in Proportion to the Effective Left Ventricular Ejection Fraction in Pressure-Volume Loop.

Left ventricular assist device (LVAD) has been saving many lives in patients with severe left ventricular (LV) failure. Recently, a minimally invasive transvascular LVAD such as Impella enables us to support unstable hemodynamics in severely ill patients. Although LVAD support increases total LV cardiac output (COTLV) at the expense of decreases in the native LV cardiac output (CONLV), the underlying mechanism determining COTLV remains unestablished. This study aims to clarify the mechanism and develop a framework to predict COTLV under known LVAD flow (COLVAD). We previously developed a generalized framework of circulatory equilibrium that consists of the integrated CO curve and the VR surface as common functions of right atrial pressure (PRA) and left atrial pressure (PLA). The intersection between the integrated CO curve and the VR surface defines circulatory equilibrium. Incorporating LVAD into this framework indicated that LVAD increases afterload, which in turn decreases CONLV. The total LV cardiac output (COTLV) under LVAD support becomes COTLV = CONLV+EFe · COLVAD, where EFe is effective ejection fraction, i.e., Ees/(Ees+Ea). Ees and Ea represent LV end-systolic elastance (Ees) and effective arterial elastance (Ea), respectively. In other words, LVAD shifts the total LV cardiac output curve upward by EFe · COLVAD. In contrast, LVAD does not change the VR surface or the right ventricular CO curve. In six anesthetized dogs, we created LV failure by the coronary ligation of the left anterior descending artery and inserted LVAD by withdrawing blood from LV and pumping out to the femoral artery. We determined the parameters of the CO curve with a volume-change technique. We then changed the COLVAD stepwise from 0 to 70–100 ml/kg/min and predicted hemodynamics by using the proposed circulatory equilibrium. Predicted COTLV, PRA, and PLA for each step correlated well with those measured (SEE; 2.8 ml/kg/min 0.17 mmHg, and 0.65 mmHg, respectively, r2; 0.993, 0.993, and 0.965, respectively). The proposed framework quantitatively predicted the upward-shift of the total CO curve resulting from the synergistic effect of LV systolic function and LVAD support. The proposed framework can contribute to the safe management of patients with LVAD.

Prediction of hemodynamics after atrial septal defect closure using a framework of circulatory equilibrium in dogs.

In patients with heart failure, atrial septal defect (ASD) closure has a risk of inducing life-threatening acute pulmonary edema. The objective of this study was to develop a novel framework for quantitative prediction of hemodynamics after ASD closure. The generalized circulatory equilibrium comprises right and left cardiac output (CO) curves and pulmonary and systemic venous return surfaces. We incorporated ASD into the framework of circulatory equilibrium by representing ASD shunt flow (QASD) by the difference between pulmonary flow (QP) and systemic flow (QS). To examine the accuracy of prediction, we created ASD in six dogs. Four weeks after ASD creation, we measured left atrial pressure (PLA), right atrial pressure (PRA), QP, and Qs before and after ASD balloon occlusion. We then predicted postocclusion hemodynamics from measured preocclusion hemodynamics. Finally, we numerically simulated hemodynamics under various ASD diameters while changing left and right ventricular function. Predicted postocclusion PLA, PRA, and QS from preocclusion hemodynamics matched well with those measured [PLA: coefficient of determination (r2) = 0.96, standard error of estimate (SEE) = 0.89 mmHg, PRA: r2 = 0.98, SEE = 0.26 mmHg, QS: r2 = 0.97, SEE = 5.6 mL·min-1·kg-1]. A simulation study demonstrated that ASD closure increases the risk of pulmonary edema in patients with impaired left ventricular function and normal right ventricular function, indicating the importance of evaluation for the balance between right and left ventricular function. ASD shunt incorporated into the generalized circulatory equilibrium accurately predicted hemodynamics after ASD closure, which would facilitate safety management of ASD closure.NEW & NOTEWORTHY We developed a framework to predict the impact of atrial septal defect (ASD) closure on hemodynamics by incorporating ASD shunt flow into the framework of circulatory equilibrium. The proposed framework accurately predicted hemodynamics after ASD closure. Patient-specific prediction of hemodynamics may be useful for safety management of ASD closure.

Prediction of haemodynamics after interatrial shunt for heart failure using the generalized circulatory equilibrium.

AimsInteratrial shunting (IAS) reduces left atrial pressure in patients with heart failure. Several clinical trials reported that IAS improved the New York Heart Association score and exercise capacity. However, its effects on haemodynamics vary depending on shunt size, cardiovascular properties, and stressed blood volume. To maximize the benefit of IAS, quantitative prediction of haemodynamics under IAS in individual patients is essential. The generalized circulatory equilibrium framework determines circulatory equilibrium as the intersection of the cardiac output curve and the venous return surface. By incorporating IAS into the framework, we predict the impact of IAS on haemodynamics.Methods and resultsIn seven mongrel dogs, we ligated the left anterior descending artery and created impaired cardiac function with elevated left atrial pressure (baseline: 7.8 ± 1.0 vs. impaired: 11.9 ± 3.2 mmHg). We established extracorporeal left‐to‐right atrial shunting with a centrifugal pump. After recording pre‐IAS haemodynamics, we changed IAS flow stepwise to various levels and measured haemodynamics under IAS. To predict the impact of IAS on haemodynamics, we modelled the fluid mechanics of IAS by Newton's second law and incorporated IAS into the generalized circulatory equilibrium framework. Using pre‐IAS haemodynamic data obtained from the dogs, we predicted the impact of IAS flow on haemodynamics under IAS condition using a set of equations. We compared the predicted haemodynamic data with those measured. The predicted pulmonary flow [r 2 = 0.88, root mean squared error (RMSE) 11.4 mL/min/kg, P < 0.001), systemic flow (r 2 = 0.92, RMSE 11.2 mL/min/kg, P < 0.001), right atrial pressure (r 2 = 0.92, RMSE 0.71 mmHg, P < 0.001), and left atrial pressure (r 2 = 0.83, RMSE 0.95 mmHg, P < 0.001) matched well with those measured under normal and impaired cardiac function. Using this framework, we further performed a simulation study to examine the haemodynamic benefit of IAS in heart failure with preserved ejection fraction. We simulated the IAS haemodynamics under volume loading and exercise conditions. Volume loading and exercise markedly increased left atrial pressure. IAS size‐dependently attenuated the increase in left atrial pressure in both volume loading and exercise. These results indicate that IAS improves volume and exercise intolerance.ConclusionsThe framework developed in this study quantitatively predicts the haemodynamic impact of IAS. Simulation study elucidates how IAS improve haemodynamics under volume loading and exercise conditions. Quantitative prediction of IAS haemodynamics would contribute to maximizing the benefit of IAS in patients with heart failure.

A three minutes supine position test reveals higher risk of spinal anesthesia induced hypotension during cesarean delivery. An observational study.

Background: Cesarean delivery is performed under spinal anesthesia, and vasodilation is the main cause for a drop in blood pressure. The compression of the aorta and inferior vena cava by the gravid uterus is of additional clinical importance. Hypotension may occur during cesarean delivery even if prophylactic infusion of phenylephrine is practiced. We have tested if a 3 minute supine observation, can identify a subset of women with decreasing systolic arterial pressure (SAP) under spinal anesthesia. Methods: We performed a prospective observational study at Oslo University Hospital on healthy pregnant women for planned cesarean delivery. Continuous measurements of calibrated invasive SAP and estimated cardiac output were recorded for 76 women in a 3 minutes measurement with the woman in the left lateral position, followed by supine position for 3 minutes. Using functional data clustering, principal component analysis and curve smoothing, to filter way noise and reduce the dimensionality of the signal, we clustered the women into separate SAP groups. Results: We identified two significantly different groups of women during supine position; one characterized by initial drop in SAP, the other showed initial increase. After spinal anesthesia, the mean SAP curve of the women in the first group showed a drop in blood pressure, which was more rapid than for the other women. A minor difference in cardiac output was observed between the two groups of women with the mean cardiac output curve for the first group being higher. Conclusions: This work indicates that supine position affect clinically relevant cardiovascular measurements in pregnant women. A simple test may identify patients with increased risk of spinal anesthesia induced hypotension.

Prediction of the impact of venoarterial extracorporeal membrane oxygenation on hemodynamics.

Although venoarterial extracorporeal membrane oxygenation (ECMO) was developed to rescue patients with cardiogenic shock, the impact of ECMO on hemodynamics is often unpredictable and can lead to hemodynamic collapse. In this study, we developed a framework in which we incorporated ECMO into the extended Guyton's model of circulatory equilibrium and predicted hemodynamic changes in response to ECMO. We first determined the cardiac output (CO) curves of left and right heart (to generate the integrated CO curve) without ECMO in eight normal and seven dogs with left ventricular dysfunction. Using the CO curves obtained and standard parameters for the venous return surface, we predicted the circulatory equilibrium under various levels of ECMO support. The predicted total flow (native left heart flow plus ECMO flow), right atrial pressure (PRA), and left atrial pressure (PLA) matched well with those measured [total flow: coefficient of determination (r(2)) = 0.99, standard error of estimate (SEE) = 5.8 ml·min(-1)·kg(-1), PRA: r(2) = 0.95, SEE = 0.23 mmHg, PLA: r(2) = 0.99, SEE = 0.59 mmHg]. Lastly, we estimated the CO curves under ECMO support from minute changes in hemodynamics induced by change in ECMO. From the CO curves estimated, we predicted the circulatory equilibrium. The predicted total flow (r(2) = 0.93, SEE = 0.5 ml·min(-1)·kg(-1)), PRA (r(2) = 0.99, SEE = 0.54 mmHg), and PLA (r(2) = 0.95, SEE = 0.89 mmHg) matched reasonably well with those measured. A numerical simulation indicated that ECMO support may cause pulmonary edema, if right ventricular function is compromised. We conclude that the proposed framework may enhance the benefit and reduce the risk of ECMO support in patients with critical hemodynamic conditions.

Tactics of antihypertensive therapy in patients with hypertonic crisis complicated with hemorrhagic stroke

To determine an optimal tactics of antihypertensive therapy in patients with hypertonic crisis complicated with hemorrhagic stroke. We examined 86 inpatients, 42 men and 44 women, aged 46-87 years, with hypertonic crisis complicated with hemorrhagic stroke. The severity of neurological deficit, parameters of cardiac output and Kaplan-Meier survival curve based on the level of arterial pressure (AP) were assessed. The best survival rate of the patients with systolic blood pressure >162 mm Hg to the 20th min from the beginning of treatment with the greater rate of its increase was established. The efficacy of antihypertensive therapy did not depend on the baseline neurological deficit. The remote survival rate did not depend on such factors as sex, age, baseline AP level, AP, frequency of heart contractions, hematoma's volume.

Rebuttal from Philip Andrew

Beard & Feigl's call for the removal of Guyton's venous return curve from teaching materials (referred to here as the Guyton–Levy venous pressure curve, VPC), is not based on any deficiency of the VPC itself but purely on Guyton's own conceptual misinterpretations thereof (Beard & Feigl, 2013). Levy resolved these misinterpretations in 1979 (Levy, 1979) and there is today no valid remaining misinterpretation. Yet Beard & Feigl, evidently unaware of the full power of the VPC when combined with the Frank-Starling cardiac output (CO) curve to form Guyton's Graphical Analysis (GGA; Guyton et al. 1973), to this day unsurpassed in its ability to model the central haemodynamics of any circulatory state, would have the baby (GGA) thrown out with the bathwater (Guyton's misinterpretations). Hoping not to put too fine a point on the matter, Beard & Feigl assert that in Guyton's original VPC experiment (Guyton et al. 1957) the artificial pump was the independent variable. In fact, the pump was downstream to the Starling resistor (SR) thus rendering pump output dependent on the hydrostatic height of the SR relative to the canine surrogate mid right atrium. The pump was adjusted manually simply to insure quantitative transfer to the canine left heart of whatever flow emerged through the SR; how much flow was entirely dependent on the throttling effect of the SR. Accordingly, the SR, not the pump, was the true independent variable governing the experiment. This in no way alters the reality that CO was the independent variable controlling right atrial pressure (RAP). As cited (Beard & Feigl, 2013), Grodins and Levy used preparations essentially identical to Guyton's (the SR was excluded) and they varied CO by simply changing the pump rate. Their VPC was similar. This not only supported the validity of Guyton's experiment and the VPC itself, but it also helped disprove Guyton's backpressure premise – if the VPC is the same with or without a SR (which is a simulated tricuspid stenosis intuitively implying backpressure), then RAP must vary due to something other than backpressure. Beard & Feigl imply the VPC and GGA are deficient for their failure to model peripheral tissue–organ haemodynamics. The VPC/GGA are models of the central circulation. Irrespective of the sundry nuances of peripheral perfusion, spent blood is presented back to the heart by the vasculature in aggregate, not in particular, and this is faithfully represented by the VPC/GGA. GGA, properly understood, exposes clinical decision making based on considerations of ‘venous return’ as the conceptual distraction it is. GGA accurately provides all the central circulatory information needed to optimally comprehend and manage clinical cardiovascular disorders. There is no clinical circumstance compelling considerations of venous return in lieu of venous pressure as all changes in venous return translate into proportionate changes in venous pressure.

Quantitative Prediction of Impact of Left Ventricular Assist Device (LVAD) on Hemodynamics

BackgroundAlthough LVAD has been saving many lives in patients with end stage heart failure, the quantitative prediction of LVAD on hemodynamics remains to be established.Theoretical analysisWe developed a framework of circulatory equilibrium where the cardiac output (CO) curve and venous return surface (VRS) were expressed as the function of right (PRA) and left atrial pressure (PLA). The CO curve is algebraically derived using the concept of ventricular arterial (VA) elastance coupling. Incorporating LVAD into the VA coupling indicates that LVAD support (COVAD) increases left ventricular (LV) afterload and decreases native CO (COLV). The total CO (COtotal) becomes COtotal=COLV+COVADEFe where EFe approximates ejection fraction. In contrast, LVAD does not change the VRS or right ventricular CO curve. Equilibrating the COtotal curve and VRS yields CO, PRA and PLA.Methods/ResultsIn 6 anesthetized, vagotomized dogs, we isolated the carotid sinuses to abolish baroreflex. We ligated coronary arteries to create LV failure and inserted LVAD. We changed COVAD stepwise from 0 to 100 ml/kg/min and predicted COtotal, PLA and PRA in each LVAD support. As shown, predicted COtotal, PLA and PRA quantitatively matched well with those measured.ConclusionThe proposed framework predicts the impact of LVAD on hemodynamics and thus contributes to the optimal management of patents on LVAD.

Anisotropic Reinforcement of Acute Anteroapical Infarcts Improves Pump Function

We hypothesize that a therapy that improves left ventricular (LV) pump function early after infarction should decrease the need for compensation through sympathetic activation and dilation, thereby reducing the risk of developing heart failure. The mechanical properties of healing myocardial infarcts are an important determinant of LV function, yet improving function by altering infarct properties has proven unexpectedly difficult. Using a computational model, we recently predicted that stiffening a large anterior infarct anisotropically (in only one direction) would improve LV function, whereas isotropic stiffening, the focus of previous studies and therapies, would not. The goal of this study was to test the novel strategy of anisotropic infarct reinforcement. We tested the effects of anisotropic infarct reinforcement in 10 open-chest dogs with large anteroapical infarcts that depressed LV pump function. We measured regional mechanics, LV volumes, and cardiac output at a range of preloads at baseline, 45 minutes after coronary ligation (ischemia), and 30 minutes later, after surgical reinforcement in the longitudinal direction (anisotropic). Ischemia shifted the end-systolic pressure-volume relationship and cardiac output curves rightward, decreasing cardiac output at matched end-diastolic pressure by 44%. Anisotropic reinforcement significantly improved systolic function without impairing diastolic function, recovering half the deficit in overall LV function. We conclude that anisotropic reinforcement is a promising new approach to improving LV function after a large myocardial infarction.

Equilibrium analysis between the venous return surface and cardiac output curve enables us to predict hemodynamic impact of percutaneous cardiopulmonary support (PCPS)

BackgroundPCPS is a vital tool in managing cardiogenic shock with respiratory failure. It remains difficult, however, to quantitatively predict the hemodynamic impact of PCPS. Theoretical analysis: We developed a circulatory equilibrium model in which cardiac output (CO) and venous pressures (right and left atrial pressures(PRA and PLA)) are determined as the intersection between the venous return (VR) surface and integrated CO curve. PCPS shifts the VR surface downward to the same extent of PCPS assisted flow (ΔCO). In contrast, PCPS increases left ventricular afterload pressure by R*ΔCO (R: arterial resistance) independent of ventricular ejection. Thus, PCPS lowers the equilibrium pulmonary CO and venous pressures. Using this model, we predicted CO and venous pressures under various levels of PCPS.Methods and ResultsIn 5 anesthetized dogs (15–20 kg), we inserted PCPS and isolated carotid sinuses with bilateral vagotomy. We measured hemodynamics (CO, PLA, PRA, and aortic pressure) under various levels of PCPS support. Predicted COs and PLA correlated well with those measured (y=0.91x+6.9, r2=0.91, n=17, y=1.03x‐0.5, r2=0.93, n=17), whereas marginally correlated in PRA (y=0.69x+1.08, r2=0.73, n=17).ConclusionWe could predict the impact of PCPS on CO and venous pressures. The proposed framework would be useful in managing patients with severely compromised hemodynamics.

Non-invasive beat-to-beat cardiac output monitoring by an improved method of transthoracic bioimpedance measurement

The report describes a method of impedance cardiography using an improved estimate of thoracic volume. The formulas and their implementation in hardware and software are explained and new shortband electrodes are described which generate a good homogeneous thoracic field. Examples of stroke volume and cardiac output curves underline the capabilities of the monitoring system “Task Force ® Monitor”. In several experiments, results are compared to thermodilution as well as to BioZ measurements: the new method excels in comparison with thermodilution and is comparable to the BioZ device. Compared to traditional electrodes, the new shortband electrodes are shown to provide better reproducibility.

Measuring Cardiac Output: Intermittent Bolus Thermodilution Method

cialist in the cardiac care unit and cardiac observation unit at UCLA Medical Center and is an assistant professor of nursing at the UCLA School of Nursing, Los Angeles, Calif. by a computer and converted into a measurement of cardiac output. Cardiac output is inversely proportional to the area under the curve. The normal cardiac output curve has a rapid smooth upstroke and a gradual downstroke (Figure 1). A small area under the curve indicates a high cardiac output. The faster blood flows through the heart, the earlier the peak and sharper the drop, because the catheter senses temperature change over a short period. A low cardiac output results in a larger area under the curve. When blood flows slowly (low cardiac output), the area under the curve (temperature change over time) is greater because the catheter senses changes in temperature over a longer period. The curves vary according to the patient’s clinical condition and according to deviations in technique (Figure 2). Concerns about contamination of prefilled syringes of injectate and proximal port of a pulmonary artery catheter located in the right atrium. In the atrium, the injectate mixes with the blood and passes through the tricuspid valve into the right ventricle. A thermistor within the catheter senses the change in blood temperature as the blood passes the catheter tip located in the pulmonary artery. A curve that shows the change in temperature over time is calculated ProtocolsforPractice

A novel framework of circulatory equilibrium.

A novel framework of circulatory equilibrium was developed by extending Guyton's original concept. In this framework, venous return (CO(V)) for a given stressed volume (V) was characterized by a flat surface as a function of right atrial pressure (P(RA)) and left atrial pressure (P(LA)) as follows: CO(V) = V/W - G(S)P(RA) - G(P)P(LA), where W, G(S), and G(P) denote linear parameters. In seven dogs under total heart bypass, CO(V), P(RA), P(LA), and V were varied to determine the three parameters in each animal with use of multivariate analysis. The coefficient of determination (r(2) = 0.92-0.99) indicated the flatness of the venous return surface. The averaged surface was CO(V) = V/0.129 - 19.61P(RA) - 3.49P(LA). To examine the invariability of the surface parameters among animals, we predicted the circulatory equilibrium in response to changes in stressed volume in another 12 dogs under normal and heart failure conditions. This was achieved by equating the standard surface with the individually measured cardiac output (CO) curve. In this way, we could predict CO [y = 0.90x + 5.6, r(2) = 0.95, standard error of the estimate (SEE) = 8.7 ml.min(-1).kg(-1)], P(RA) (y = 0.96x, r(2) = 0.98, SEE = 0.2 mmHg), and P(LA) (y = 0.89x + 0.5, r(2) = 0.98, SEE = 0.8 mmHg) reasonably well. We conclude that the venous return surface accurately represents the venous return properties of the systemic and pulmonary circulations. The characteristics of the venous return surface are invariable enough among animals, making it possible to predict circulatory equilibrium, even if those characteristics are unknown in individual animals.

A critical analysis of the view that right atrial pressure determines venous return.

A. C. Guyton pioneered major advances in understanding cardiovascular equilibrium. He superimposed venous return curves on cardiac output curves to reveal their intersection at the one level of right atrial pressure (Pra) and flow simultaneously consistent with independent properties of the heart and vasculature. He showed how this point would change with altered properties of the heart (e.g., contractility, sensitivity to preload) and/or of the vasculature (e.g., resistance, total volume). In such graphical representations of negative feedback between two subdivisions of a system, one input/output relationship is necessarily plotted backward, i.e., with the input variable on the y-axis (here, the venous return curve). Unfortunately, this format encourages mistaken ideas about the role of Pra as a "back pressure," such as the assertion that elevating Pra to the level of mean systemic pressure would stop venous return. These concepts are reexamined through review of the original experiments on venous return, presentation of a hypothetical alternative way for obtaining the same data, and analysis of a simple model.

The role of the vasculature in regulating venous return and cardiac output: historical and graphical approach.

To review the physiology of cardiac output regulation by the peripheral vasculature. This will enable the clinician to understand and manage the complex circulatory changes in various forms of shock, and in other common altered circulatory states encountered in anaesthetic practice. Articles were obtained from a Medline review (1966 to present; search terms: shock, venous return, cardiac output) and a hand search (Index Medicus). Other sources include review articles, personal files, and textbooks. At steady state, cardiac output is equal to venous return (VR). Venous return depends on mean systemic pressure (PMS), which is the pressure in the peripheral vasculature driving blood flow to the heart, right atrial pressure (PRA), and the resistance to venous return (RV). When considering VR, PRA is the downstream pressure to VR, and not simply an indirect measure of the volume status. The pressure gradient for VR is, therefore, PMS-PRA, and in a system obeying Ohm's Law, [formula: see text] Shock and other altered circulatory states cause changes in both VR and cardiac function. The circulation can be conveniently described by a venous return and a cardiac output curve. By drawing these curves for each clinical situation, a clear understanding of the altered circulatory state is obtained, and treatment options can be clearly defined. The peripheral circulation controls cardiac output in many clinical conditions. Manipulation of the peripheral circulation is as important to the successful treatment of shock and other altered circulatory states, as is the manipulation of cardiac output.

Effect of dual-chamber pacing on systolic and diastolic function in patients with hypertrophic cardiomyopathy Acute doppler echocardiographic and catheterization hemodynamic study

Objectives. This study sought to evaluate prospectively the acute hemodynamic effect of dual-chamber pacing by using a combined hemodynamic approach of high fidelity pressure and Doppler velocity measurements.Background. Dual-chamber pacing has been proposed recently as an alternative in the symptomatic treatment of patients with hypertrophic obstructive cardiomyopathy. Although early reports documented a decrease in left ventricular outflow tract gradient and symptomatic improvement, questions remain about the hemodynamic effects of dual-chamber pacing on systolic and diastolic function.Methods. Twenty-nine patients with hypertrophic cardiomyopathy underwent a combined cardiac catheterization and Doppler echocardiographic study during normal sinus rhythm and P-synchronous pacing at various atrioventricular (AV) intervals. High fidelity pressure measurements of left ventricular inflow and left atrial pressures, ascending aortic pressure, thermodilution cardiac output and Doppler mitral flow velocity curves were obtained to evaluate both systolic and diastolic left ventricular function.Results. During AV pacing at the shortest delay of 60 ms, there was a significant decrease in cardiac output (p < 0.05) and peak positive dP/dt (p < 0.05), an increase in mean left atrial pressure (p < 0.05) and a prolongation of τ, the time constant of relaxation (p < 0.05), compared with that during normal sinus rhythm. During pacing at the optimal AV delay (longest AV interval with pre-excitation), there was a similar trend, with deterioration in both systolic and diastolic function variables but of lesser magnitude than that during pacing at the shortest AV intervals. The deterioration in both systolic and diastolic function was present in 21 patients with and 8 without left ventricular outflow obstruction. There was a modest decrease in left ventricular outflow tract gradient from 73.3 ± 45.0 (mean ± SD) to 61.3 ± 40.5 mm Hg (p = 0.03) during dual-chamber pacing at the optimal AV delay compared with that during normal sinus rhythm.Conclusions. The acute effect of pacing the right atrium and ventricle may be detrimental to both systolic and diastolic function of the left ventricle, particularly at the short AV intervals. Further studies of the long-term effects of dual-chamber pacing in carefully performed randomized studies are needed.

Issues in Methods and Measurement of Thermodilution Cardiac Output

Criterion-related validity of the thermodilution cardiac output technique for cardiac output measurement has to have a high correlation (r = .91 to .98) with the direct Fick method, the gold standard of cardiac output measurement. Issues that can affect validity of the measurements include the position of the pulmonary artery catheter, the rate of injection of the indicator solution, the volume and temperature of the injectate, the timing of the injection of indicator solution during the respiratory cycle, the position of the subject, and the presence of concomitant infusions. Variation in measurement can be limited by considering the delivery system for the indicator solution, by recording time-temperature cardiac output curves, and by considering normal biologic variations.

Asymmetrical septal hypertrophy in patients with hypertension: a type of hypertensive left ventricular hypertrophy or hypertrophic cardiomyopathy combined with hypertension?

To determine whether asymmetrical septal hypertrophy (ASH) in patients with essential hypertension (HT) is a type of hypertensive left ventricular (LV) hypertrophy or hypertrophic cardiomyopathy (HCM) combined with HT, we investigated a group of 7 hypertensive patients with ASH compared with 12 HCM patients and 10 healthy controls using radionuclide angiography and right ventricular endomyocardial biopsy. The LV time-volume curve and its first and second derivative curves were constructed from cardiac output and time-activity curves constructed by combined forward and reverse-gating from the R wave. The LV wall thickness and ejection fraction were significantly greater in both the HT and HCM groups than in the control group, whereas there were no differences in these indices between the HT and HCM groups. Rapid filling volume index and rapid filling fraction showed significantly lower values in the HCM group than in the control group (p < 0.005). In contrast to the HCM group, these indices in the HT group did not differ from those in the control group. The time to peak filling rate was prolonged in the control, hypertension, and HCM groups in increasing order. Histopathological study revealed a higher incidence of myocardial cell disarray in the HCM than in the HT group. The above results suggest that ASH in hypertensive patients is a type of hypertensive LV hypertrophy.

Thermodilution estimation of cardiac output at high flows in anesthetized horses

SUMMARY The purpose of this study was to compare the thermodilution technique for estimation of cardiac output with the indocyanine green dye dilution technique at flows between 10 and 39 L/min in halothane-anesthetized horses. The estimation of area of dye dilution cardiac output curves was made by using the fore-’n-aft (fa) triangle method. This shorthand technique was compared with logarithmic exponential extrapolation and summation (extrapolated area), using 64 cardiac output curves. Then, 256 simultaneous thermodilution measurements were compared with dye dilution measurements calculated by use of the fa technique. Forty milliliters of iced 0.9% NaCl solution containing 15 mg of indocyanine green dye was used as the indicator. This was delivered in &lt; 1 second to the right atrium, using a power injector. A thermistor positioned in the pulmonary artery detected the thermal indicator. Blood was withdrawn from the carotid artery through a densitometer cuvette to measure the dye concentration. The fa estimations of area were higher than those determined by use of extrapolated area. A multiplicative adjustment of 0.837 was estimated. On average, thermodilution estimates of cardiac output exceeded the adjusted fa determinations. Using a weighted linear regression, we determined the following calibration adjustment: thermal dilution cardiac output/1.048 = indocyanine green dye dilution cardiac output.