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The Cause of Pressure Sores
Published in J G Webster, Prevention of Pressure Sores, 2019
The arteries carry high pressure blood from the heart to the arterioles. They have a peak pressure (systolic pressure) of about 120 mm Hg and minimal pressure (diastolic pressure) of 70 mm Hg during each heart cycle. Their pulse pressure, the difference between the systolic and diastolic pressures, is normally about 50 mm Hg. To do this they have strong walls consisting of three layers: an endothelial lining, a middle layer with elastic tissue and smooth muscle, and a outer layer of connective tissue. The arterioles also have three layers and have pressures of about 40 mm Hg. By the end of the arterioles, just before the capillaries, they have a mean pressure between 30–38 mm Hg with a pulse pressure of about 5 mm Hg. Their smooth muscle layer undergoes vasoconstriction or vasodilation to regulate the amount of blood flow to the capillaries. These responses are controlled by sympathetic nerves that discharge in a manner that keeps a continuous tension in the smooth muscle layer of the arterioles. The rate at which they discharge determines the amount of constriction or tone in the vessels. These nerves are controlled by the groups of neurons in the medulla of the brain that are collectively called the vasomotor center. The activity of this center is affected by many factors: blood concentrations of O2 and CO2, excitatory inputs from pain pathways, and inhibitory inputs from aortic baroreceptors to name a few. Ganong (1989) gives a complete description.
Cardiovascular System:
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
The arteries move blood away from the heart and, with the exception of the pulmonary artery, carry oxygenated blood. The elastic fibers within the arterial wall allow for high compliance or “expandability.” The elastic arteries, or conducting arteries, include the aorta and its major branches. They range in diameter from 1 to 2.5 cm and contain a high proportion of elastin within the tunica layers. These arteries act as a pressure reservoir that expands as it receives blood from the left ventricle in systole and then recoils during diastole, helping to smooth out the pulsatile flow seen in these vessels. The thick wall and high percentage of elastic tissues help the vessel withstand the high and changing pressures. The peak arterial pressure (or systolic pressure) is seen during ventricular ejection, while the minimal arterial pressure (or diastolic pressure) occurs just before ejection begins. The difference in systolic and diastolic pressure is called the pulse pressure. It is dependent on the stroke volume ejected by the ventricle, as well as the vessel’s elastic properties that determine arterial compliance. With aging, the arterial vessel walls can stiffen (arteriosclerosis) and result in a higher pulse pressure. This will be discussed in more detail in Chapters 6 and 11.
Hypertension and Correlation to Cerebrovascular Change: A Brief Overview
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
Heba Kandil, Dawn Sosnin, Ali Mahmoud, Ahmed Shalaby, Ahmed Soliman, Adel Elmaghraby, Jasjit S. Suri, Guruprasad Giridharan, Ayman El-Baz
Invasive blood pressure monitoring also offers beat to beat visual display of the arterial waveform, which measures the rapid changes in pressure over the measurement epochs. The waveform display provides information such as steepness and narrowness of systolic stroke, dicrotic notch, and wave reflections. Pulse pressure is the difference between the peak arterial pressure measurement and the diastolic pressure at the trough. MAP is the area under the curve divided by the width of a single cardiac cycle. MAP provides a measurement that is less affected by wave reflection than the systolic and diastolic readings [14], [21].
Effect of the level of effort during resistance training on intraocular pressure
Published in European Journal of Sport Science, 2019
Jesús Vera, Raimundo Jiménez, Beatríz Redondo, Alejandro Torrejón, Carlos Gustavo De Moraes, Amador García-Ramos
A wrist digital automatic blood-pressure monitor (RX3, Omron, Hoofddorp, The Netherlands), which has been clinically validated (Cuckson, Moran, Seed, Reinders, & Shennan, 2004), was used to measure BP before and after each training set. Blood-pulse pressure (BPP) was calculated as the difference between systolic and diastolic blood pressure reading.
Acute differences in blood lipids and inflammatory biomarkers following controlled exposures to cookstove air pollution in the STOVES study
Published in International Journal of Environmental Health Research, 2022
Ethan S. Walker, Kristen M. Fedak, Nicholas Good, John Balmes, Robert D. Brook, Maggie L. Clark, Tom Cole-Hunter, Robert B. Devlin, Christian L’Orange, Gary Luckasen, John Mehaffy, Rhiannon Shelton, Ander Wilson, John Volckens, Jennifer L. Peel
The generalizability of our results is also limited by the study population. The healthy, young adults in our study do not represent the wide spectrum of cookstove users around the world who follow countless cultural, dietary, and cookstove-use practices. In addition, our study design limited us to assessing short-term exposures to cookstove air pollution, whereas cookstove users are often exposed to cookstove air pollution daily over the course of their lives. Although the external validity of our study is limited, studies of this nature help us understand the underlying health impacts of household air pollution exposures. Atherosclerosis and advanced cardiovascular disease progress over the course of many years, yet the facilitating events take place acutely and repeatedly. Here and in previous publications from the present study, we have observed evidence that short-term exposures to particulate matter air pollution emitted from cookstoves can lead to acute cardiovascular changes in young, healthy adults. Repeated particulate matter air pollution exposures may result in an underlying increase in cardiovascular disease risk (Brook et al. 2010), and in the case of higher triglycerides and inflammatory biomarkers, may lead to an increased risk of the progression of atherosclerosis (Gonzalez and Selwyn 2003; Libby and Ridker 2004; Talayero and Sacks 2011). The connection between the treatments in our study and cardiovascular disease risk is further supported by the differences we observed in hemodynamic indices. We have previously reported higher systolic blood pressure (Fedak et al. 2019), pulse wave velocity, and central pulse pressure (Walker et al. 2020) 24 hours after the treatments compared to control. Blood pressure, pulse wave velocity, and central pulse pressure are clinical indicators of cardiovascular disease and can change acutely through inflammatory pathways that impact endothelial function and vascular tone (Brook et al. 2010; Tomiyama and Yamashina 2010). Together, the results from our study show a consistent story that air pollution emitted from cookstoves is capable of acutely impacting multiple indicators of vascular function and cardiovascular disease risk. We recommend that future field studies assess the impact of cookstove interventions on biomarkers and indicators of vascular function to complement our findings.