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The pathophysiology of sepsis

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by Gemlee Gemlee (New) New

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Why septic patient become hypotensive, tachycardia , tachypnoec,hypoxaemia and pale and explain the pathophysiology of each please

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Rose_Queen is a BSN, MSN, RN and specializes in OR, education.

4 Followers; 4 Articles; 8,911 Posts; 104,599 Profile Views

Welcome to AN! We do request that you show us what your research has shown you so far. Do you have a pathophysiology book to use as a jumping off point?

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are you asking for us to do your homework? you can find that in your textbook and sometimes google may help. I suggest you to read and understand it, in the future many of your patients will present all or some of these s/s and you will have to be able to recognize them, now it is your time to learn to do so.

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It would be helpful if you showcase where you are lost regarding sepsis pathophys, that way we can redirect you. So you go first, then we'll chip in.

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Thanks, micro organisms get into the blood stream which will enhance immunity response to produce cytokines that will disorganise the systemic circulation as it cause the venodilation. Thus reduce the after load and increase the cardiac output and preload . So as a result hypotension then tachycardia as a heart compensatory mechanism. Decreased venous perfusion cause pale skin . Reduced oxygenation due to consolidation caused by panini is can result hypoxaemia. I don't know my concept is on right track

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203 Posts; 5,985 Profile Views

Great. Vasodilation is the key word once the pathogens have triggered immune response. Remember the left side of the heart needs to overcome resistance in order to pump blood to the system. In sepsis, arterial dilation means vascular resistance is low so the left side has minimal to low resistance to overcome, thus cardiac output is decreased. Further, venodilation causes blood to pool in the rest of the body so that blood is not returning to the right side. Therefore, there isn't enough blood reaching the lungs for oxygenation (hypoxemia) and also not enough to pump around. And as you have mentioned, compensatory mechanism kicks in. Because there is less oxygen in the blood, the brain tells the respiratory center to breathe even faster (tachypnea). With tachycardia, understand that INITIALLY vasodilation will cause a rise in HR so as to compensate, but EVENTUALLY will decrease if compensation is not corrected.

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