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Pathophysiology of Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Jacob Cao, John O'Sullivan, Sean Lal
Both cardiac preload and afterload are reduced. Preload lowering is achieved through natriuresis and osmotic diuresis, with magnetic resonance imaging studies showing significant reduction in skin sodium concentration after a brief treatment with dapagliflozin. Afterload lowering is due to reductions in systolic and diastolic blood pressures, which is mediated through total fluid loss, in addition to reduced arterial stiffness and improvement in endothelial health. Although classical diuresis also offers offloading of the heart, SGLT2 inhibitors may offer the additional benefit of maintaining intravascular volume, thereby minimizing risks of renal injury.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Afterload is the force opposing ventricular ejection; in the left ventricle, this is the opposition given by the aortic diastolic pressure. Changes in systemic vascular resistance (SVR) caused by peripheral vasoconstriction or dilation will affect afterload. Systemic vascular resistance will increase with peripheral vasoconstriction, and the patient who feels cool to touch will have an increased left ventricular afterload. The myocardium has to work harder to push the blood out of the ventricle, and will therefore require more oxygen as it uses more energy. In health, this is not a problem, but in the failing heart, pharmacological therapy is aimed at reducing the left ventricular afterload by enabling arteriolar vasodilation in order to reduce the oxygen requirements of the myocardium. Problems with the heart valves, for example, aortic stenosis, increase the work of the left ventricle, as it needs to generate an increased pressure to squeeze blood though the stenotic valve. This, over time, will damage the ventricular myocardium and the damaged heart valves may need to be replaced.
Mechanical Events of the Cardiac Cycle
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
Three main factors – preload, afterload and myocardial contractility of the heart – determine the volume of blood ejected by the ventricles during systole and the ejection pressure. Preload is the degree of stretch of ventricular muscle fibres at the end of ventricular filling, as represented by the end-diastolic volume. This is the basis of Starling's law of the heart: the diastolic length of ventricular fibres determines their force of contraction. Afterload is the left ventricular wall stress developed during ventricular ejection and reflects the force opposing the shortening of the ventricular myocytes during contraction. Myocardial contractility is the intrinsic ability of the myocardial cells to develop force at a given fibre length, independent of preload and afterload.
Effect of Combined Grape Seed Extract and L-Citrulline Supplementation on Hemodynamic Responses to Exercise in Young Males
Published in Journal of Dietary Supplements, 2023
Brian Shariffi, Katherine Dillon, Trevor Gillum, William Boyer, Sean Sullivan, Esther Lee, Jong-Kyung Kim
Along with our findings that GSE, L-citrulline, and its combination supplementations increased TVC, it seems reasonable to assume that NO-induced vasodilation occurred in contracting skeletal muscles. These results are similar with those reported by other studies that GSE or L-citrulline supplementation reduced peripheral vasoconstriction (21,36). Our study also found that these supplementations augmented exercise-induced increases in cardiac output at heavier workloads compared to the placebo treatment. However, there were no additive effects on cardiac output responses. This increase in cardiac output may be attributed to a reduced afterload related to concomitant increase in TVC. It was not clear why increases in cardiac output and TVC were not enhanced at the two lower workloads. Although speculative, substantial increase in production of NO derived from contracting skeletal muscle during heavier workloads as well as dietary supplementations is likely to be sufficient in reducing afterload and the corresponding increase in cardiac output (8,21,37). However, it should be noted that there were no additive benefits toward cardiac and vascular function.
Antihypertensive treatment and risk factors for syncope in asymptomatic aortic stenosis patients with hypertension
Published in Clinical and Experimental Hypertension, 2022
Meihua Wu, Ping Gu, Qianqiang Cao, Aibin Gong, Wenliang Tan, Dezhi Hong
AS is a common valvular disease, affecting 2 to 4% of adults older than age 65 years (13). It is a progressive disease with a long asymptomatic phase, but once symptoms develop, the prognosis is poor (14). Systemic HTN is present in about 9%-76% of patients with AS in different studies (1). Despite the recognition that HTN is an important medical problem that requires effective treatment to minimize cardiovascular morbidity and mortality, there has been reluctance to treat (or at least adequately treat) HTN in patients with AS (15). This reluctance stems from the now outdated notion that obstruction at the valve level is the overwhelmingly dominant cause of increased LV load and that, in the face of this fixed afterload, cardiac output cannot be augmented (16). However, it is misleading to think of AS as a disease with “fixed afterload.” Indeed, increased vascular afterload serves as an additional load on the left ventricle and is associated with increased hypertrophic remodeling and LV dysfunction in patients with AS (1).Increased global LV load – measured as the Zva(see above) – also portends a worse outcome (17). In fact, a growing body of literature has reported that a high percentage of patients with significant AS do take antihypertensive and vasoactive medications without evident adverse effects (18–20). Among the 158 AS patients included in our study, ninety patients had hypertension. The prevalence of hypertension was 56.9%; 77 of them were using antihypertensive agents; 36% of patients with treated HTN had normal blood pressures (<140/90 mmHg); about 29% had blood pressures ≥150/100 mmHg.
Roles of arterial pressure volume index and arterial velocity pulse index trajectories in risk prediction in hypertensive patients with heart failure with preserved ejection fraction
Published in Clinical and Experimental Hypertension, 2020
Jindong Wan, Sen Liu, Yi Yang, Dan Wang, Fei Ran, Siwei Xia, Shuangtao Ma, Jixin Hou, Peng Zhou, Yun Sun, Peijian Wang
There are several possible explanations for present findings. Firstly, clinical trials have emphasized that increase in artery stiffness was a major contributor to cardiac diastolic dysfunction, ultimately promoting the development of HFpEF (8,26). In this regard, our study explicitly demonstrated the prognostic significance of arterial stiffness based on the API/AVI trajectories in hypertensive patients with HFpEF. Secondly, the workload on the heart may be increased in patients with higher API/AVI trajectories, resulting in left ventricular hypertrophy and dysfunction. Likewise, afterload-induced changes can be elevated in hypertensive patients, which may lead to left ventricular diastolic dysfunction. This is consistent with the biological evidence that arterial stiffness-related markers may exert structural and functional influences on left ventricular remodeling and HFpEF progression (32,33). Our study provides a unique opportunity to understand association between API/AVI and established indicators of cardiac overload (PP, BNP, and SVI), suggesting that API and AVI are involved in the pathophysiology of HFpEF. Thirdly, the risk of coronary-related events was the greatest for patients with very high API/AVI trajectory in all HFpEF patients. This might be due to that low diastolic pressure caused by elevated arterial stiffness measured via API/AVI resulted in decline in coronary perfusion. Hence, the significance of monitoring API/AVI for cardiovascular outcomes in HFpEF are varied.