In medicine we worship at the altar of SBP. In ICU the MAP reigns supreme. But too often the poor old DBP is an afterthought, & it’s crying out for our attention.

A short 🧵 on the clinical utility of the ugly duckling of blood pressures, the Diastolic Blood Pressure 🎉

1/ It makes sense to consider first what determines DBP?

At end systole, aortic pressure begins to exponentially decay as the ejected SV/pressure wave propagates down the arterial tree. Uninterrupted, it will continue to drop until the mean circulatory filling pressure is reached

The Pv-aCO2 gap is an easily obtained measure that serves as a marker of impaired cardiac output/tissue perfusion, yet seemingly few of us use it in practice

A short 🧵 on ΔCO2, its potential benefits & some pitfalls

#Hameodynamics #FOAM

https://twitter.com/norfolk_tim/status/1482769404102381568

The Pv-aCO2 gradient (ΔCO2) is simply the partial pressure of CO2 in venous blood (mixed or central venous) - the partial pressure of CO2 in arterial blood.

Normal values are ≤ 6mmHg (0.8kPa)

Values > 6mmHg suggest a low CO or impaired microvascular tissue perfusion

Doc 1: There’s a big swing on their A-line, shall I give more fluids?

Doc 2: Well given that they’re spontaneously breathing, there’s no real evidence to support PPV here 🤷‍♂️

- A recently overheard conversation, prompting this 🧵 on PPV in the spontaneously breathing patient. The ∆ between systolic & diastolic pressures is the pulse pressure (PP) & it is determined by the compliance of the aorta and the ventricular stroke volume (SV).

Whilst aortic compliance reduces with age, beat-to-beat changes in PP occur predominately due to changes in SV.