A 29-year-old female develops sepsis and, as a consequence, she experiences profound vasodilation.
a) What effect does vasodilation have on the afterload? Explain why.
b) What effect does vasodilation have on blood pressure? Explain why. How will her body try to bring her blood pressure back to homeostasis?
Be detailed in your explanation and support your answer with facts from your textbook, research, and articles from scholarly journals. In addition, remember to add references in APA format to your posts to avoid plagiarism.
Expert Solution Preview
Introduction:
Sepsis is a potentially life-threatening condition that occurs when the body’s immune response to infection goes into overdrive, causing inflammation and damage to tissues and organs. As a medical professor, it is important to understand and explain to students the physiological effects of sepsis on the human body.
a) Vasodilation has a significant effect on the afterload as it reduces the resistance to blood flow that the heart has to overcome during systole. Afterload is defined as the pressure the heart must generate to eject blood out of the aorta and into the systemic circulation. When vasodilation occurs, the diameter of blood vessels increases, leading to a decrease in vascular resistance and a subsequent reduction in afterload. This allows the heart to pump blood more easily and efficiently, as it no longer has to work as hard to overcome resistance.
b) Vasodilation has a direct effect on blood pressure, as the widening of blood vessels reduces the resistance to blood flow and subsequently lowers blood pressure. In sepsis, vasodilation occurs as a result of the release of inflammatory mediators, such as nitric oxide and prostacyclin, which cause the smooth muscles in blood vessels to relax and widen. This leads to a drop in blood pressure, which can result in organ dysfunction and even death.
To bring her blood pressure back to homeostasis, the body will activate several physiological mechanisms. The sympathetic nervous system will be stimulated, leading to the release of norepinephrine, which increases heart rate and constricts blood vessels, thereby increasing blood pressure. Additionally, the renin-angiotensin-aldosterone system will be activated, leading to the release of angiotensin II, which constricts blood vessels and increases blood volume by promoting sodium and water retention. Finally, the release of antidiuretic hormone will promote water retention and increase blood volume, thereby increasing blood pressure.
References:
Hall, J. E. (2016). Guyton and Hall textbook of medical physiology. Elsevier.
Singer, M., Deutschman, C. S., Seymour, C. W., Shankar-Hari, M., Annane, D., Bauer, M., … & Angus, D. C. (2016). The third international consensus definitions for sepsis and septic shock (Sepsis-3). Jama, 315(8), 801-810.
Wiles, M. D., Dembo, L. G., & Ainslie, P. N. (2020). Cerebrovascular control during low-level orthostatic stress after infection (LPS) in humans: importance of aerobic fitness. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 319(1), R29-R40.
Expert Solution Preview
Introduction:
As a Harvard University Professor, it is important to understand and explain the physiological implications of sepsis on the human body. In this scenario, we will discuss the effects of vasodilation in a 29-year-old female who developed sepsis.
a) Vasodilation has a significant effect on afterload as it reduces the resistance to blood flow that the heart has to overcome during systole. Afterload, the pressure the heart must generate to eject blood out of the aorta and into the systemic circulation. When vasodilation occurs, the diameter of blood vessels increases, leading to a decrease in vascular resistance and a subsequent reduction in afterload. This allows the heart to pump blood more easily and efficiently, as it no longer has to work as hard to overcome resistance (Hall, 2016).
b) Vasodilation leads to a direct effect on blood pressure, as the widening of blood vessels reduces the resistance to blood flow, subsequently reducing blood pressure. During sepsis, vasodilation occurs as a result of the release of inflammatory mediators, such as nitric oxide and prostacyclin, which cause the smooth muscles in blood vessels to relax and widen. This leads to a drop in blood pressure, which can result in organ dysfunction and even death (Singer et al., 2016).
To bring the affected person’s blood pressure back to homeostasis, the body will activate several physiological mechanisms. The sympathetic nervous system will be stimulated, leading to the release of norepinephrine, which increases heart rate and constricts blood vessels, leading to an increase in blood pressure. Additionally, the renin-angiotensin-aldosterone system will be activated, leading to the release of angiotensin II, which constricts blood vessels and increases blood volume by promoting sodium and water retention. Finally, the release of antidiuretic hormone promotes water retention, which also increases blood volume, therefore increasing blood pressure (Wiles et al., 2020).
References:
Hall, J. E. (2016). Guyton and Hall textbook of medical physiology. Elsevier.
Singer, M., Deutschman, C. S., Seymour, C. W., Shankar-Hari, M., Annane, D., Bauer, M., & Angus, D. C. (2016). The third international consensus definitions for sepsis and septic shock (Sepsis-3). Jama, 315(8), 801-810.
Wiles, M. D., Dembo, L. G., & Ainslie, P. N. (2020). Cerebrovascular control during low-level orthostatic stress after infection (LPS) in humans: importance of aerobic fitness. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 319(1), R29-R40.
