Cardiovascular physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The tendency for blood to return to the heart from the peripheral circulation can be characterized by the venous return curves described by Guyton. In an experimental animal preparation (Figure 4.34), a bypass pump replaces the right ventricle and blood enters the pump via a collapsible tube and is returned to the pulmonary artery. The pump maintains a pressure of −10 to −20 mmHg. The right atrial pressure is adjusted by raising or lowering the segment of the collapsible tubing. When the right atrial pressure in this preparation is raised to 7 mmHg, venous return falls to zero, circulation stops and pressure equalizes throughout the systemic blood vessels. This occurs because blood collects in the compliant venous capacitance vessels. The pressure at which venous return ceases is the MSFP. This corresponds to the degree of filling of systemic circulation and is determined by the blood volume and venous capacitance. The MSFP is normally about 7 mmHg in humans. As the right atrial pressure is reduced to below MSFP, venous return increases up to about 5 L/min in humans when the right atrial pressure is zero. Therefore, venous return decreases linearly with increases in right atrial pressure between zero and the MSFP (Figure 4.35). Venous return is proportional to the difference between MSFP and right atrial pressure, which is the hydrostatic pressure gradient promoting venous return. In this range of right atrial pressure (i.e., 0–7 mmHg), venous return can be defined by the following equation:
Venous Return and Vascular Function
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The tendency for blood to return to the heart from the peripheral circulation can be characterized by the venous return curves described by Guyton. In an experimental animal preparation (Figure 30.3), a bypass pump replaces the right ventricle and blood enters the pump via a collapsible tube and is returned to the pulmonary artery. The pump maintains a pressure of −10 to −20 mmHg. The right atrial pressure is adjusted by raising or lowering the segment of the collapsible tubing. When the right atrial pressure in this preparation is raised to 7 mmHg, venous return falls to zero, circulation stops and pressure equalizes throughout the systemic blood vessels. This occurs because blood collects in the compliant venous capacitance vessels. The pressure at which venous return ceases is the MSFP. This corresponds to the degree of filling of systemic circulation and is determined by the blood volume and venous capacitance. The MSFP is normally about 7 mmHg in humans. As the right atrial pressure is reduced to below MSFP, venous return increases up to about 5 L/min in humans when the right atrial pressure is zero. Therefore, venous return decreases linearly with increases in right atrial pressure between zero and the MSFP (Figure 30.4). Venous return is proportional to the difference between MSFP and right atrial pressure, which is the hydrostatic pressure gradient promoting venous return. In this range of right atrial pressure (i.e. 0–7 mmHg), venous return can be defined by the following equation:
Interventional Therapies for Essential Hypertension
Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei in Manual of Hypertension of the European Society of Hypertension, 2019
The creation of an AV fistula results in blood flow parallel to the systemic circulation, leading to a reduction in systemic vascular resistance and cardiac afterload (15). It is well known that peripheral AV fistulae in haemodialysis patients are accompanied by decreases in BP and peripheral resistance (16,17). However, BP reduction due to the shunt in turn leads to sympathetic activation. The increase in venous return and sympathetic activation result in an increase in cardiac output. The percentage of the cardiac output that the shunt holds needs therefore to reach a threshold over which any increase in systemic resistance and cardiac output fail to maintain the baseline BP, eventually leading to its reduction. On the other hand, the increased cardiac preload leads to higher right atrial and pulmonary capillary wedge pressure that may attenuate the baroreceptor reflex (along with sympathetic activation) as well as trigger the release of natriuretic peptides. Furthermore, a central AV anastomosis reduces effective arterial blood volume to a new baseline without depleting other volume capacitance spaces, and thus without neurohormonal activation. This is of particular interest for the ageing aorta, where the stress-strain curve shifts to the left; after the anastomosis, for any increase in intravascular volume, a milder increase in BP is expected, restoring arterial compliance (18).
In search of mechanisms to explain the unquestionable benefit derived from sodium-glucose cotransporter-2 (SGLT-2) inhibitors use in heart failure patients
Published in Postgraduate Medicine, 2023
Angel Lopez-Candales, Khalid Sawalha, Betty M. Drees, Nicholas B. Norgard
To better explain stressed and unstressed blood volume better, let us review some physiology. Veins contain about 70% of TBV in comparison to arteries where it contains approximately 30%[31]. Guyton el at. described a model of venous return in 1955 along with the factors that influence its physiology, he highlighted three variables that independently affect the venous return: (a) the vascular resistance, (b) the mean systemic pressure, and (c) the right atrial pressure[32]. Among all these three variables, the mean systemic pressure is the least in getting the attention it deserves; this may be due to the complex and intricate system that makes the attempts to define its importance difficult. It is basically the pressure measured in the vascular system if the blood flow were to cease[33]. It is determined by the TBV present in the venous system and the compliance of that vascular bed to dilate of constrict. Physiologically speaking, it is the required volume of fluid to fill the vascular bed where it exerts a force on the vessel walls, and this is what is known as UBV. Now, any volume that will exert a rising pressure (above that normal one) on the vascular bed is known as SBV[33]. Therefore, it is related to venous constriction and dilation and that veno-constriction shifts blood volume from the unstressed to the stressed pool, resulting in increased pulmonary venous pressure, pulmonary edema, and thus HF.
The influence of Body Roundness Index on sensorial block level of spinal anaesthesia for elective caesarean section: an observational study
Published in Journal of Obstetrics and Gynaecology, 2020
Betul Kozanhan, Omer Bardak, Mahmut Sami Tutar, Sibel Ozler, Munise Yildiz, Ibrahim Solak
A higher sensory block level may contribute to circulatory instability and lead hypotension after spinal anaesthesia in parturients. Circulatory regulation influenced by a blockade of the sympathetic nervous system producing decreases in both venous return and systemic vascular resistance. Increased abdominal content with the pregnant uterus and visceral adipose tissue are the further risk factors for an event of hypotension following neuraxial anaesthesia, as a result of widespread displacement of the intra-abdominal content, and vascular compression that exacerbates the aortocaval compression. It is known that higher BMI is associated with higher intra-abdominal pressure (Abdel-Razeq et al. 2010; Fuchs et al. 2013). In the present study, hypotension occurred in 55.2% of the patients and bradycardia occurred in 24.2% of the patients. We found a significant correlation between BRI and the maximum sensory block level; however, the episodes of hypotension were unrelated to BRI. This result may be due to the potential metabolic and cardiovascular changes linked with increased BRI (Chang et al. 2015; Zhang et al. 2016).
Acute effects of glossopharyngeal insufflation in people with cervical spinal cord injury
Published in The Journal of Spinal Cord Medicine, 2018
Malin Nygren-Bonnier, Tomas A. Schiffer, Peter Lindholm
Previous studies have described the mechanics and pointed out the risks involved when performing glossopharyngeal breathing.9,10 During glossopharyngeal breathing, high intrathoracic pressure may develop with a concurrent depressant effect on the arterial pressure. This will have a similar effect to a valsalva manoeuvre, where a person voluntarily strains to increase the intrathoracic pressure, which may cause orthostatic syncope from the reduction in venous return.11 Many reports have shown that significant hemodynamic abnormalities occur during glossopharyngeal breathing. Arterial blood pressure falls, and heart rate (HR) increases in healthy individuals.11,12 In a study by Loring et al.,13 the transpulmonary pressures increased up to 80 cm of H2O with glossopharyngeal breathing, and the intrapulmonary pressures increased up to 109 of cm H2O. Those results indicated that some healthy individuals are able to withstand repeated insufflations to transpulmonary pressures higher than within normal range of pressure. Autonomic dysreflexia has been shown to occur in patients with CSCI,14 and it is possible that these patients may be more susceptible to reduction in blood pressure during GI compared to healthy people.
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