Pathophysiology of sepsis: Sepsis is a spectrum that ranges from mild (SIRS) to moderate (septic shock), to severe (MSOD).
In sepsis, the primary mechanism of damage is the invasion of a pathogen, typically a bacteria. When the bacteria enters the bloodstream, or the interstitial space, WBCs recognize it and release Nitric Oxide, causing the blood vessels to become permeable. The purpose of this is to allow WBCs to move from the interstitial space into the bloodstream. This works fine if the infection is localized and WBCs are able to overcome the pathogens. However, if the WBCs are outnumbered and pathogens are able to gain the upper hand, the infection can become systemic (spread throughout the body's circulatory system). This results in a situation where the increased permeability of the blood vessels leads to leakage of fluid into the interstitial space, causing hypovolemia. As a result we get Systemic Inflammatory Response Syndrome (SIRS).
*** Remember: HR x SV = CO + SVR = MAP
In SIRS, there is a decrease in systemic vascular resistance, which leads to the activation of compensatory mechanisms; namely, the increase in cardiac output to compensate for the hypotensive state. We get an increase in HR and SV in an attempt to increase BP. While this is successful, the patient is said to be in a compensatory state of shock. However, this is very energy expensive and eventually will fail without medical intervention. Once compensatory mechanisms fail and BP again drops, the patient is said to be in decompensating shock. In SIRS, the disruption in oxygen to cells, due to third spacing and relative hypovolemia, leads to anaerobic cellular metabolism, and a state of metabolic acidosis. The body compensates for this by increasing respiratory rate to blow off excess CO2. As a result we see increase in RR and decrease in ETCO2.
The key to managing these patients is to:
Recognize signs early.
Address hypotension.
Protect the cells from acidosis (administer O2).
Signs of SIRS include a combination of 2 or more of the following:
Temperature >38.0 or <36.0
HR >90
SBP <90 systolic (may be above 90 if the patient is still compensating effectively).
Respiratory rate >20
ETCO2 <30
Additionally alterations in LOC may be noted, as may elevations in BGL.
MSOD (Multisystem organ dysfunction):
There is another problem for the body aside from just perfusion deficits. The destruction of pathogens in the bloodstream leads to an accumulation of cellular debris. These debris damage the tunica intima of the vessels, leading to the activation of clotting factors. Platelets begin to aggregate in areas of damage in order to repair the tunica intima. This is fine on a localized scale, but remember, at this point we are dealing with a systemic problem. The body only has a finite number of readily available clotting factors, which means we eventually end up in a state of disseminated intravascular coagulation (DIC).
Once the clotting factors are depleted, platelets break free and begin to block microcirculation, leading to damage to the kidneys, liver, etc. Many of the patients who get to this point will need dialysis.
This is why early recognition is key.
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