Week 6 Discussion: 29-Year-Old Female Develops Sepsis

Week 6 Discussion Foruma 29 Year Old Female Develops Sepsis Following

Week 6: Discussion Forum A 29-year-old female develops sepsis following a bacterial infection from a leg wound. As a consequence, she experiences profound vasodilation. For the prompt, explain in depth: What effect does vasodilation have on afterload and why? What effect does vasodilation have on blood pressure and why? How would her body compensate to bring her blood pressure back to homeostasis? 250 words- 2 references

Paper For Above instruction

Vasodilation, which involves the relaxation and widening of blood vessels, profoundly impacts cardiovascular dynamics, especially during septic conditions. In this scenario, the patient's profound vasodilation results in a significant decrease in systemic vascular resistance. This decrease directly influences afterload, which is the resistance the ventricles must overcome to eject blood during systole. Reduced systemic vascular resistance from vasodilation leads to a lower afterload, making it easier for the heart to pump blood, but simultaneously, it decreases the workload and pressure the heart must generate to eject blood effectively (Bickley, 2017). Consequently, with decreased afterload, the heart can pump more freely, although this may be detrimental if systemic blood pressure drops significantly.

The primary effect of vasodilation on blood pressure is a reduction. Blood pressure depends on cardiac output and systemic vascular resistance; when vasodilation reduces vascular resistance, blood pressure falls accordingly (Guyton & Hall, 2016). This hypotension can impair tissue perfusion, leading to organ dysfunction. To counteract this and restore blood pressure, the body's compensatory mechanisms activate. Baroreceptors located in the carotid sinuses and aortic arch detect decreased blood pressure and respond by increasing sympathetic nervous system activity. This response results in vasoconstriction of undilated vessels, increased heart rate, and enhanced myocardial contractility, all aimed at restoring blood pressure to homeostatic levels (Ganong, 2015). Additionally, hormonal responses such as the renin-angiotensin-aldosterone system are activated, leading to vasoconstriction and increased blood volume through sodium and water retention, thus further aiding in stabilizing blood pressure (Guyton & Hall, 2016). These combined responses facilitate the return of blood pressure to normal levels, ensuring adequate perfusion despite the vasodilatory challenge presented by sepsis.

References

• Bickley, L. S. (2017). Bates' Guide to Physical Examination and History Taking. Wolters Kluwer.
• Ganong, W. F. (2015). Review of Medical Physiology. McGraw-Hill Education.
• Guyton, A. C., & Hall, J. E. (2016). Textbook of Medical Physiology. Elsevier.