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Discussion

Question about Septic Shock

Hello all!

I am studying for the CEN and have been using the med ed videos by Jeff Solheim (love them!). I was re-reviewing the shock module today and have a question about hypodynamic sepsis that I can't find the answer to.

Jeff says that in early sepsis (hyperdynamic sepsis) you are vasodilated, of course, as a result of circulating inflammatory mediators and increased capillary permeability. In hypodynamic sepsis, he says the body becomes SNS and alpha stimulated as a compensatory response to the initial hypotension. But even though their SVR is increased, they are still hypotensive. How is this the case? In septic shock, the patient is typically not hypovolemic, so vasoconstriction should fix the BP, correct? Also, since the treatment of the profound hypotension in septic shock is vasopressors, why would vasopressors even work if the body is already SNS and alpha stimulated?

Also, in anaphylactic shock, what causes the bronchoconstriction?

So confused. Please help. Thanks for your input!

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    I haven't seen the videos you're referencing, but Solheim may be using nomenclature that doesn't accurately describe the physiology. Hyper- and hypodynamic are terms universally applied to cardiac wall motion on echocardiograms. Indeed, a hypodynamic heart (e.g. HF) may not be effectively pumping at all especially against high SVR, but a hyperdynamic heart doesn't just become hypo.

    It also sounds like he's oversimplified some the mechanisms at play that result in hypotension like the vasodilatory byproduct of bacteremia and even bacterial cell wall lysis following antibiotic administration.

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    The first treatment for hypotension in septic shock is fluids. (30ml/kg given as a bolus over 0.5-1 hour). The main hemodynamic factor which causes decreased BP is profound arterial vasodilation. Therefore, you must fill the tank and see if the patient is fluid responsive before starting any vasopressors.

    But even though their SVR is increased, they are still hypotensive.

    I think what he means is that although the SVR is increased initially as a compensatory mechanism to bring up the BP, eventually this mechanism fails and you have a shock state.

    Leukotrienes cause the bronchoconstriction. Medscape: Medscape Access

    The alpha effect includes tachycardia, increased strength of contraction, and increased cardiac output and therefore BP. However, the vasodilation in septic shock is so profound that this compensatory mechanism may fail. The vasopressors/constrictors clamp down on the vasculature and create some counterpressure to the bloodflow aka increased SVR and thereby increase BP. This is why volume is so important. You must fill the tank.

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