This damage may predispose survivors to chronic hypertension, underscoring the importance of long-term cardiovascular follow-up for this population. This results in an increased heart rate and force of contraction, along with widespread vasoconstriction, which can elevate systemic vascular resistance and systolic blood pressure significantly.
How Sepsis Inflammation Alters Blood Pressure Through Vascular and Nervous System Responses
While vasopressor medications are standard for treating hypotensive shock, managing hypertension in sepsis focuses on addressing the root cause. Episodes of severe sepsis and septic shock can cause lasting damage to the cardiovascular system, including endothelial injury and autonomic nervous system dysregulation.
The sympathetic nervous system surges, releasing norepinephrine and epinephrine, while the renin-angiotensin-aldosterone system (RAAS) becomes highly active. This massive release of inflammatory mediators, such as tumor necrosis factor-alpha and interleukins, causes blood vessels to dilate excessively and become more permeable.
How Sepsis Inflammation Alters Blood Pressure Through Vascular and Nervous System Responses
Vasoconstriction in non-essential vascular beds raises peripheral resistance. While hypotension, or low blood pressure, represents a classic hallmark of progressive sepsis, the relationship between this dangerous condition and hypertension, or high blood pressure, is more complex than one might assume.
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