Responses needed -150 words- one citation for just one peer
Physiology discussion – the one about “A 29-year-old female develops sepsis following a bacterial infection from a leg wound. As a consequence, she experiences profound vasodilation.”
Responses must promote a discussion either by sharing prior knowledge and experiences, making meaningful connections with course content, asking meaningful questions, or challenging viewpoints.
Student #1:
Sabreen Zayed
Hi everyone,
Blood vessels widen, or expand, because of the smooth muscles in the vessel walls relaxing. Substances such as nitric oxide are made during sepsis, leading to wide vasodilation. This impacts the cardiovascular system in multiple ways. First, the force the heart must resist to pump blood into the arteries is reduced through vasodilation. The heart has an easier time pumping blood out because there is less barrier to blood flow when the blood arteries widen. This resistance reduction immediately decreases the afterload. Vasodilation also reduces blood pressure. “Endothelial dysfunction, with reduced vasodilator capacity, has long been linked to elevated blood pressure” [1Links to an external site.]. The amount of blood the heart pumps as well as the resistance in the blood arteries determine blood pressure. Blood pressure falls as a result of the arteries widening and lowering resistance. This explains why sepsis sufferersVasodilation also brings about a reduction in blood pressure. Blood pressure is influenced by blood vessel resistance as well as the volume of blood the heart pumps. Blood pressure lowers when the arteries enlarge because there is less resistance. Because their blood vessels are unable to sustain the usual pressure required for healthy circulation, persons with sepsis frequently experience dangerously low blood pressure. The body triggers many compensatory processes in reaction to this reduction in blood pressure. “These data indicate that vasodilators stimulate TRPV4 channels, leading to Ca2+-dependent activation of nearby TMEM16A channels in endothelial cells to produce arterial hyperpolarization, vasodilation, and reduced blood pressure.”(1) Heart rate and cardiac output increase as a result of the sympathetic nervous system being activated and releasing chemicals such as adrenaline (epinephrine). By holding onto water and sodium, the kidneys contribute to elevated blood pressure and blood volume. During sepsis, these systems cooperate to raise blood pressure and keep crucial organ blood flow sufficient.
references
1. Watson T, Goon PK, Lip GY (2008) Endothelial progenitor cells, endothelial dysfunction, inflammation, and oxidative stress in hypertension. Antioxid Redox Signal 10:1079–1088 doi: 10.1089/ars.2007.1998 [PubMedLinks to an external site.] [CrossRefLinks to an external site.] [Google ScholarLinks to an external site.]
Mata-Daboin A, Garrud TAC, Fernandez-Pena C, Peixoto-Neves D, Leo MD, Bernardelli AK, Singh P, Malik KU, Jaggar JH. Vasodilators activate the anion channel TMEM16A in endothelial cells to reduce blood pressure. Sci Signal. 2023 Nov 14;16(811):eadh9399. doi: 10.1126/scisignal.adh9399. Epub 2023 Nov 14. PMID: 37963195; PMCID: PMC10694922.
Student #2:
Vivi Nguyen
Sepsis is a serious complication that can arise from an infection, occurring when chemicals released into the bloodstream to combat the infection trigger widespread inflammatory responses. This inflammation can lead to a series of changes that may damage multiple organ systems, potentially causing them to fail.
Vasodilation, which is the widening of blood vessels, increases blood flow through those vessels (Ramanlal & Gupta, 2021). This process reduces afterload, which refers to the total load on the heart during ventricular contraction, including the volume of blood in the ventricle and the resistance in the arteries. As systemic vascular resistance decreases due to vasodilation, the heart faces less resistance when pumping blood through the aortic valve into the systemic circulation.
The circulatory system consists of the heart and blood vessels, including arteries, veins, and capillaries. When arteries and arterioles dilate, both arterial blood pressure and heart rate decrease. Baroreceptors located within blood vessels help regulate blood pressure by sending signals to the cardiovascular center. If blood pressure rises, these receptors stimulate the parasympathetic nervous system, reducing cardiac output. Simultaneously, sympathetic stimulation of peripheral arterioles decreases, resulting in further vasodilation.
In response to sepsis, the body undergoes vasodilation, triggering homeostatic regulation mechanisms. These autoregulatory processes involve chemical signals and myogenic responses that help restore the vascular system to its normal state (Betts et al., 2017).
1. Betts, J. G., Desaix, P., Johnson, E., Johnson, J. E., Korol, O., Kruse, D., Poe, B., Wise, J. A., Womble, M., & Young, K. A. (2017). Anatomy and physiology. OpenStax, Rice University.
2. Ramanlal, R., & Gupta, V. (2021). Physiology, vasodilation. StatPearls Publishing.
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