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.
When asking if a pt is fluid responsive (FR), we’re asking if ⬆️ preload will ⬆️ SV. Observing a ∆PP with a ∆preload can help us try to answer this.
Pulse pressure variation (PPV) is the diff. between the max/min PP (as a % of the mean), occurring over a respiratory cycle.
Ventilation requires changes in intra-thoracic pressure (ITP), and this ∆ITP, in turn affects preload.
PPV allows us to see if these ventilation-induced changes lead to a change in SV, hinting at where pts lie on their Starling curve, and if they are likely to be FR.
Spontaneous ventilation (SpV) causes a -ve ITP & tends to ⬆️ preload; mechanical ventilation (MV) causes a +ve ITP & tends to ⬇️preload.
In each case, the size of the ∆preload, relates to the size of the ∆ITP.
This needs to be considered when interpreting PPV in practice.
During MV, a PPV >12% has been shown to accurately predict FR (sens 88%; spec 89%) as long as:
1) In health the resp system is very compliant, so tidal breathing may cause inadequate ∆ITP
2) In hypovolaemic states, a ⬇️ITP may not ⬆️preload due to collapse of the great veins (maximal venous return is already achieved)
A final caveat… for both MV & SpV: in the presence of RV/LV impairment, ventilation can significantly affect SV irrespective of preload conditions, leading to high PPV/false +ve’s
Specificity is thus significantly reduced and PPV may be of limited value 😕
So back to the original question… in the absence of RV/LV dysfunction, a high PPV in a SpV pt means it’s highly likely they’ll be FR.
Of course the likes of @msiuba@icmteaching & @ThinkingCC won’t forgive me if I don’t mention that being FR doesn’t necessarily = needs fluid!
Hope this is of use, & may even help people avoid pitfalls I know I’ve fallen for!
For far more detailed explanations please read @PrXaMonnet review article:
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 🎉
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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 rate of the decay is known as the time constant (τ) - a concept we’re familiar with from respiratory physiology.
Just like in the lungs, it’s the product of arterial compliance (C) x arterial resistance (R)
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
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
ΔCO2 is primarily determined by total CO2 production (VCO2), cardiac output (CO) and the complex relationship between pCO2 and total blood CO2 content (CCO2).
It can be conceptualised mathematically using the Fick equation