China
Africa
Explore chapters and articles related to this topic
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Preload is important, as there is a relationship between the amount of blood in the ventricle at the end of diastole and the amount of blood ejected during systole (stroke volume). This relationship is described by Starling’s law of the heart, which states that as the amount of blood returning from the veins to the ventricle at the end of diastole increases, the stretch of the ventricular myocardium increases and therefore the strength of the next contraction is greater. A useful analogy is an elastic band; the further it is stretched, the harder it springs back. This means that the more blood flows into the ventricles, the more blood is pumped out, i.e. as the left ventricular end diastolic volume increases, so does the stroke volume (see Figure 6.7). This relationship is evident in the healthy heart, but for those that have heart failure, the ability to deal with increased preload is reduced. This is discussed later in the chapter.
Interdependence Between Cardiac Function, Oxygen Demand, and Supply
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Joseph S. Janicki, Karl T. Weber, Ponnambalam Sundram
I would like to emphasize one thing regarding our results in the normal, isolated dog heart. Even though the duration of systole and, hence, the total force integral were decreased as contractile state was increased, there was a concomitant increase in the rate of force development which resulted in a greater myocardial oxygen consumption ((MV̇O2)). Therefore, in the normal heart an increase in (MV̇O2) with positive inotropic agents is always expected despite a reduction in the duration of systole. In addition, depending on the type of inotropic agent and its dose, heart rate and systolic blood pressure may not change to any great extent. Consequently neither duration, heart rate, nor blood pressure would be a valid noninvasive predictor of (MV̇O2). This is further emphasized by the findings in patients with chronic heart failure which demonstrated that (MV̇O2) did not increase following the administration of positive inotropic agents. This was primarily the result of a concomitant decrease in end-diastolic volume. This reduction effectively offset the metabolic cost of the inotrope-induced increase in the rate of force development. Obviously, such alterations in volume could not be predicted by duration of systole, heart rate, or blood pressure.
Pressure–Volume Loop of the Left Ventricle
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In diastole, the left ventricular volume rises from 60 mL at the end of systole to the end-diastolic volume of 130 mL, and the ventricular pressure rises from 5 to 10 mmHg. During isovolumetric ventricular contraction, the pressure increases to 80 mmHg before the aortic valve opens. During the ejection phase, the ventricle contracts and ejects the stroke volume of 70-mL blood against the afterload of increasing aortic pressure. Ventricular pressure rises during the ejection phase to 120 mmHg and then falls to 100 mmHg at the end of systole when the aortic valve closes again. During isovolumetric relaxation, the ventricular pressure falls once more to the end-systolic point. The area enclosed by the pressure–volume curve (the shaded area in Figure 26.1) reflects the external work done by the left ventricle in each cardiac cycle.
Resveratrol Attenuates Sepsis-Induced Cardiomyopathy in Rats through Anti-Ferroptosis via the Sirt1/Nrf2 Pathway
Published in Journal of Investigative Surgery, 2023
Youcheng Zeng, Guodong Cao, Liang Lin, Yixin Zhang, Xiqing Luo, Xiaoyu Ma, Akelibieke Aiyisake, Qinghong Cheng
Cardiac function assessment of each rat group was completed using echocardiography. The rats were anesthetized at the 24th hour after CLP, and cardiac ultrasonography was performed immediately after skin preparation. To take M-mode echocardiographic measurements, an ultrasound machine (PHILIPS EPIQ7C, USA) with a 15-MHz transducer probe was employed. The left ventricular end diastolic volume (LVEDV), left ventricular end systolic volume (LVESV), as well as the left ventricular internal dimension diastole (LVIDd) and systole (LVIDs) were measured. Additionally, the following algorithms were used to compute the markers of left ventricular systolic function, left ventricular ejection fraction (LVEF) and left ventricular shortening fraction (LVFS):
Physiological characterization of an arginine vasopressin rat model of preeclampsia
Published in Systems Biology in Reproductive Medicine, 2022
Sapna Ramdin, Thajasvarie Naicker, Virushka Pillay, Sanil D. Singh, Sooraj Baijnath, Blessing N Mkhwanazi, Nalini Govender
Earlier studies also linked AVP to arterial blood pressure regulation (Jablonskis and Howe 1993; Song and Martin 2006; Li et al. 2012). The elevations in both systolic and diastolic blood pressure in our study throughout pregnancy in the PAVP group, suggests that arginine vasopressin stimulates the renin-angiotensin aldosterone system (RAAS). This results in vasoconstriction, which is mediated via the V1a receptor and consequently increases peripheral resistance and systemic blood pressure as observed in our study (Qian 2018). Myocardial atrial contraction results in an atrial-induced increase in end-diastolic pressure, which subsequently enhances ventricular contraction. Arginine vasopressin increases the impact of norepinephrine and Ang II on cardiac muscle and blood vessels thus altering hemodynamic function (Lee et al. 2003), and negatively affects myocardial contraction (Goldsmith 2005; Goldsmith and Gheorghiade 2005). Chronic hypertension results in diastolic dysfunction and consequent left ventricular hypertrophy thereby reducing cardiac compliance (Lorell and Carabello 2000). This results in a higher diastolic pressure–volume relationship where even minor elevations in left ventricular end-diastolic volume induces a significant rise in left ventricular end diastolic pressure (Gutierrez and Blanchard 2004). The pronounced effect of AVP on diastolic pressure may be due to the exaggerated interaction of AVP with the V1A and V2 receptors on peripheral blood vessels (Goldsmith 2005; Goldsmith and Gheorghiade 2005).
The Pathophysiology of Afterload Mismatch and Ventricular Hypertrophy
Published in Structural Heart, 2021
The major function of any muscle, whether the tensor tympani, the biceps, or the myocardium, is to generate force that creates movement. The heart muscle uses that function to deliver adequate blood (cardiac output) to the body’s tissues while maintaining tolerable filling pressure. Cardiac output in turn is the product of heart rate and stroke volume. Stroke volume is dependent upon inherent ventricular end diastolic volume (larger subjects have larger hearts), preload, afterload and contractility. Contractility is the innate ability of the myocardium to generate force, while afterload is that force against which the myocardium must contract, and preload is a sarcomeric length-dependent mechanism for augmenting force development. The following discusses these properties concentrating primarily on afterload excess and its consequence: reduced stroke volume and/or the development of concentric ventricular hypertrophy.