bradycardia and CVP

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A patient has extreme bradycardia, 30 bpm, with a 3rd degree AV block. Cardiac output is reduced due to slow frequency. Contractility and TPR are increased as compensation but what happens to CVP and why?

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

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This is homework in that I am a student nurse (in Holland) and am trying to figure this out... the question I posed myself. I am on holiday at the moment and therefore not at college or at work with people immediately available to ask and am having trouble finding an answer in my books and on the internet.I stumbled upon this site and thought why not post here and see if anyone can help... Does this justify my question???

Most of the information I have found deals with cardiogenic shock where the cardiac output is reduced due to stroke volume reduction as is the case with infarction for example and compensation is with increased frequency. In this case CPV increases though I am going round in circles trying to understand the mechanisms which cause this... And when bradycardia is the cause of reduced cardiac output and we have Adams Stokes syndroom do we also speak of cardiogenic shock?

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Specializes in GICU, PICU, CSICU, SICU.

Hey ChrisSmith,

When I'm reading your question my mind immediately falls to the technical aspect of CVP measuremets. You mention certain key signs that provide you a basis of what's happening.

CVP is measured in the vena cava superior or right atrium depending on catheter length. However the assumption we make is that CVP equals RAP (right atrial pressure) and that RAP equals RVEDP (right ventricular end diastolic pressure). And in fluid status we then make the assumption that RVEDP equals RVEDV (right ventriclar end diastolic volume) and we then assume left and right side of the heart are equal to eachother. A bunch of assumptions which in my humble opinion make CVP as a value on its own very dodgy at best. But thus far my ranting against CVP ^^. Keep in mind that the principle here is that of communicating vessels without obstructions to block the signal.

Now take a look at what happens during third degree AV-block you lose the synchrony between atrium and ventricle. This means that in a majority of the atrial contractions this leads to a contraction against the closed valve between atrium and ventricle (tricuspid valve) leading to canon A-waves on your CVP-tracing. Other than that consider the effect bradycardia has on the filling time of your heart.

These two above hints will allow you to derive your own conclusion what happens to your CVP in 3rd degree AVB.

And to answer your question concerning Adam Stokes Syndrome and cadiogenic shock. In my opinion it does. Shock is defined as "inadequate delivery of substrates and oxygen to meet the metabolic needs of the tissues". If you pass out from bradycardia I think that qualifies as your brain not receiving enough oxygen and substrates to meet its metabolic needs and the cause is cardiogenic in origin.

I'm wondering are you not working with PGO (problem oriented education) in your nursing school? Normally these questions would arise during your PGO session and an answer would have been searched for.

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I was struggling with applying more basic concepts and eventually found a nice simple explanation here: CV Physiology: Central Venous Pressure

Thanks for your reply Belgian which was also very helpfull.

I am just a few weeks into my CCU training. They work with 'competentie gericht onderwijs' (competence orientated education??) but here that is applied more on the workfloor than in the classroom.

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