Interspecies Extrapolation of Toxicological Data
Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach in Health Risk Assessment, 2017
Cardiac output is defined as the volume of blood pumped by each ventricle of the heart per minute. There is considerable evidence that cardiac output is related to metabolic rate (Guyton, 1971) and that metabolic rates across species are related to the three fourths power of body weight (Kleiber, 1961; Holt et al., 1968; White et al., 1968, and Schmidt-Nielsen, 1970). The most commonly assumed scaling law for cardiac output has the form:where Q is a species-independent allometric constant. Percent of cardiac output distributed to different organs is approximately constant across species (Arms and Travis, 1988). Thus, cardiac output, Q¡, to tissue group i has the form:where Q is a species-independent allometric constant.
Right heart catheterization: Cardiac output, vascular resistance, shunt detection, and quantification
Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead in Cardiovascular Catheterization and Intervention, 2017
With the widespread switch from transfemoral to transradial access for left heart catheterization, right heart catheterization, including endomyocardial biopsy, is increasingly performed via an antecubital vein. Apart from operator experience and preference, certain conditions make a SVC approach preferable. Such conditions are as follows: suspected femoral vein/iliac vein thrombosis, renal vein thrombus, inferior vena cava (IVC) filter, and anomalous IVC. Other conditions, such as massive dilation of the rightsided chambers, severe tricuspid or pulmonary regurgitation, and pulmonary hypertension, are technically easier to assess by a SVC approach. The PAC (Figure 9.1) is advanced through the right atrium (RA), the right ventricle (RV), and the PA until a PA occlusion pressure is reached (Figure 9.2). The static column of blood between the tip of the PAC and the pulmonary vein will transmit the pressure from the left atrium (LA). During diastole, when the mitral valve is open, the measured pressure corresponds to the left ventricular diastolic pressure (Figure 9.2). A prerequisite of a correct measurement is that the pulmonary venous pressure exceeds the pulmonary alveolar pressure. This is more likely the case when the catheter tip is directed into the lower lobe. The lung tissue between the tip of the catheter and the left heart results in damping (2-4 mmHg) and delay (100-150 msec) of the pressure wave in the pulmonary capillary wedge tracing compared with the left ventricular (LV) or LA pressure (Figure 9.3). Cardiac output measurements are usually performed by thermodilution or by the Fick method. Thermodilution is more accurate in normal and high output states, whereas the Fick method is more accurate in low output states, valvular regurgitation, or intracardiac shunts. Shunt detection and quantification is complementary to echocardiography results. Echocardiographic findings should be reviewed before performing right heart catheterization so that the invasive procedure can be tailored toward unresolved and specific questions. This will allow the investigator to shorten the oximetry run and plan a potentially valuable pharmacologic intervention or volume load.
Shock
Ian Greaves, Keith Porter, Chris Wright in Trauma Care Pre-Hospital Manual, 2018
Hypovolaemic shock remains the greatest single contributor to early trauma mortality and, in many respects, reflects the final common pathway for all forms of shock. Cardiac output is dependent on stroke volume and heart rate. Stroke volume, the amount of blood ejected by the left ventricle in one contraction, is influenced by preload, myocardial contractility and afterload. Preload, or diastolic filling, is affected by venous blood pressure, venous tone and the volume of circulating blood. An absolute or relative reduction in the volume of circulating blood can thus reduce cardiac output. Stroke volume is also dependent on myocardial contractility and afterload. Increased myocardial contractility is a compensatory mechanism in hypovolaemia. However, the hypoxaemia and acidaemia associated with hypoperfusion depress myocardial contractility. Similarly, left ventricular afterload, the resistance opposing myocardial ejection of blood, is closely linked to systemic vascular resistance. Increased systemic vascular resistance is also a compensatory mechanism that may, if prolonged, result in both reduced tissue perfusion and increased afterload. Cardiac output is also related to heart rate. Increased heart rate is a compensatory mechanism in hypovolaemia but the potentially adverse consequence is that the increased heart rate is at the expense of the duration of diastole and cardiac filling and, in due course, results in reduced preload.
Mechanisms Involved in Angiotensin II Induced Increases in Cardiac Output in Pithed Rats
Published in Clinical and Experimental Hypertension. Part A: Theory and Practice, 1991
Regis R. Vollmer, Susan A. Meyers-Schoy, Riccardo R. Marinelli
This study was conducted to determine the mechanisms by which angiotensin II (Ang-II) acutely increases cardiac output. Pithed Sprague-Dawley rats were prepared for continuous measurement of cardiac output by electromagnetic flowmetry. Ang-II (31 – 1000 ng/kg, i.v.) produced dose-related increases in cardiac output, heart rate and stroke volume. Although the heart rate increases were abolished by beta-adrenoceptor blockade, the cardiac output responses were unchanged due to an offsetting increase in stroke volume. The constancy of the cardiac output response following beta-adrenoceptor blockade suggested that Ang-II increased cardiac output by constricting venous smooth muscle and thereby increasing venous return. This conclusion is supported by the observation that Ang- I I produced marked increases in 1 eft ventri cul ar end diastolic pressure that paralleled the increases in cardiac output. In fact, based on volume loading with Tyrode's solution, the changes in left ventricular end diastolic pressure produced by Ang-I1 should have resulted in even greater increases in cardiac output. However, it appears that the significant rise in peripheral resistance to Ang-cardiac output. In addition, the Ang-II-induced elevations in II tended to counter the effects of increased venous return on cardiac output. In addition, the Ang-II-induced elevations in cardiac output were not altered by alpha-adrenoceptor blockade. Therefore, catecholamines do not play a role in mediating the Ang-II effects. The results of this study support the conclusion that Ang-II is capable of increasing cardiac output by constriction of venous smooth muscle.
Maternal Weight, Hemodynamics, and Preeclampsia
Published in Hypertension in Pregnancy, 1997
Thomas R. Easterling, Barbara C. Schmucker, Stacy Selke, Steven P. Millard
Objectives: To evaluate the relationship between the obesity, elevated cardiac output, and the development of preeclampsia. Methods: Maternal weight, mean arterial pressure, and cardiac output were analyzed from 9 preeclamptic, 81 gestationally hypertensive, and 89 normotensive pregnant women at 23 weeks gestation, 34 weeks gestation, and 6–8 weeks postpartum. Data were gathered prospectively and longitudinally as part of a previously described investigation. Cardiac output was measured by Doppler technique. Data were analyzed by multiple logistic regression. The data for cardiac output, weight, and mean arterial pressure were first modeled controlling for the effect of the parameter most strongly associated with preeclampsia. The data were modeled a second and third time controlling for the other two parameters. Results: Elevated cardiac output, mean arterial pressure, and maternal weight at 23 weeks and postpartum were each associated with the development of preeclampsia. After controlling for the effects of cardiac output, neither maternal weight nor mean arterial pressure were independently associated with the development of preeclampsia. After controlling for maternal weight, elevated cardiac output remained independently associated with the development of preeclampsia. Conclusions: Increased maternal weight and elevated cardiac output are each associated with the development of preeclampsia. While elevated cardiac output has an effect independent of maternal weight, we were unable to demonstrate that maternal weight has an independent effect. Given the association between hyperinsulinemia, obesity, hypertension, and increased cardiac output in nonpregnant patients, a potential association between hyperinsulinemia, increased cardiac output, and the development of preeclampsia deserves further investigation
Measurement of Cardiac Output by Impedance Cardiography in Patients with Myocardial Infarction: Comparative Evaluation of Impedance and Dye Dilution Methods
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 1976
S. Gabriel, J. H. Atterhög, L. Orö, L. G. Ekelund
The cardiac output was measured simultaneously by the impedance cardiography and dye dilution methods in 10 patients with acute myocardial infarction 2–3 weeks after admission to the Coronary Care Unit. The impedance cardiac output was on the average 9.7% higher than the dye dilution cardiac output. The repro-ducibility of impedance cardiac output was 4.1%, compared with 5.1% for the dye dilution method. The study showed a satisfactory reliability of impedance in predicting the relative change of cardiac output in response to tilting from the supine to the 30d` head-up position, to a 10d` head-down position, and to the intravenous administration of propranolol.
Related Knowledge Centers
- Heart Rate
- Stroke Volume
- Ultrasound
- Heart
- Ventricle
- Mean Arterial Pressure
- Pulse Pressure