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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Invasive treatment is needed for patents with symptoms from significant outflow tract gradients 50 mm Hg or higher, even with medical therapy. Surgical myectomy can provide low death rates during surgery and excellent results. An alternative, used for older patients and those at high surgical risk, is percutaneous catheter alcohol septal ablation. Any drug that reduces preload decreases the size of the heart chambers and makes the signs and symptoms worse. These drugs include diuretics, nitrates, ACE inhibitors, and ARBs. Vasodilators also worsen ventricular diastolic function by increasing the outflow tract gradient, resulting in reflex tachycardia. The inotropic drugs worsen outflow tract obstruction. They do not relieve high end-diastolic pressure and can cause arrhythmias. These drugs include catecholamines and digitalis glycosides. A newer drug that may be beneficial is mavacamtem, an oral cardiac myosin inhibitor. The drug also reduces LV outflow tract obstruction and increases exercise tolerance.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Central venous pressure monitoring (CVP) is helpful for those who have complex fluid management requirements, as they help evaluate fluid status and right ventricular function. The pressure measures right atrial pressure, but also reflects right ventricular end diastolic pressure, as the AV valves open in diastole. Fluid challenges described earlier in this chapter may be repeated if the CVP is low or normal with a reduced BP to ensure circulating volume is adequate. Central venous pressure is normally between 3–8mmHg, but in clinical practice it may be maintained up to 12mmHg to ensure optimum ventricular preload. Those who do not respond to fluid challenge may require inotropic support of the circulation. Factors that may cause a rise in CVP include: Heart failure.Cardiac tamponade.Tension pneumothorax.Vasoconstriction (caused by drugs such as adrenaline or as part of the sympathetic response to poor cardiac output).COPD.Tricuspid valve problems.
Critical Care and Anaesthesia
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Rajkumar Rajendram, Alex Joseph, John Davidson, Avinash Gobindram, Prit Anand Singh, Animesh JK Patel
What are the cardiovascular effects of releasing the aortic cross-clamp?The removal of the aortic cross-clamp is associated with a significant reduction in systemic vascular resistance and a consequent decrease in the mean arterial pressure. The blood vessels in the previously ischaemic areas are severely dilated because of the accumulation of metabolites such as adenosine, lactate, and CO2 during the time of ischaemia. This promotes shift in blood flow and volume into those previously under-perfused areas causing central hypovolaemia. There is subsequently washing off the said metabolites, exacerbating hypotension.Reactive hyperaemia also ensues following unclamping due to smooth muscle relaxation, thus facilitating higher flows in areas after removal of the aortic clamp.Left ventricular end-diastolic pressure decreases significantly and myocardial perfusion increases. However, decreased myocardial contractility may be an issue due to acidosis after prolonged clamping time (increased lactate and PaCO2).The blood flow to area proximal to the clamp site reduces to levels of pre-clamping relatively quickly.
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).
HDL therapy today: from atherosclerosis, to stent compatibility to heart failure
Published in Annals of Medicine, 2019
C.R. Sirtori, M. Ruscica, L. Calabresi, G. Chiesa, R. Giovannoni, J.J. Badimon
While there are no clinical studies directly addressing the effects of apoA-I or AIM on clinical HF, two studies have examined two different aspects of HDL therapy. The first [135] employed gene therapy. The selective HDL raising AAV8 A-I gene transfer was performed at 12 weeks of age in male LDLr–/– mice. In order to obtain pressure overload, two weeks later, mice were treated by transverse aortic constriction (TAC) or sham operation. Gene therapy led to a rise of HDL-cholesterol of 1.47 fold and 1.45 fold in TAC operated and sham treated mice, respectively. A significantly lower mortality was noted in the AAV8 AI TAC mice compared to controls (HR for mortality of 0.543; 95% CI: 0.282–1.05). Heart weights, and in particular atrial weights, were significantly reduced in the AAV8 A-I TAC mice. A significant reduction of lung weights were found and, upon microscopic evaluation, there was clear indication of reduced apoptosis (–46.7%) in AAV8 AI TAC mice vs controls and marked reduction in the nitrotyrosine positive areas. Capillary density and relative vascularity were higher in gene transfected mice with a prompt decrease of interstitial and perivascular fibrosis. Morphological changes were accompanied by significantly improved diastolic function with lower end-diastolic pressure.
Epigallocatechin gallate (EGCG) attenuates myocardial hypertrophy and fibrosis induced by transverse aortic constriction via inhibiting the Akt/mTOR pathway
Published in Pharmaceutical Biology, 2021
Yue Cui, Yongqiang Wang, Gang Liu
As described previously (Liu et al. 2013), the changes in cardiac function were assessed by observing hemodynamics. After mice were anaesthetized by isoflurane inhalation, the right carotid artery was visualized the intubated with a Midro-Tip catheter (Millar) which was connected to a pressure sensor. The catheter was inserted into the left ventricle which was confirmed by the alteration of the pressure curve plotted by the Powerlab 4/25 Biological Analysis system. The left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP), mean arterial pressure (MAP), the maximum rate of left ventricular pressure decay (−dp/dt), and mean flow velocity (Vmean) were measured and recorded.