Welcome back to the tasty morsels of critical care podcast.
In the main we get excited about systolic dysfunction. We obsess over the ejection fraction with numbers like EF of 12% being reproduced recurrently in handover sheets. But this is to neglect what constitutes the vast majority of the time of cardiac cycle in those with sensible heart rates.
It has become clear that a lot of cardiac dysfunction occurs during this phase of relaxing and we neglect it at our peril.
In terms of terminology heart failure with preserved ejection fraction is the preferred term. This gets abbreviated to the wonderful HFpEF which always makes me think of Hufflepuff from Harry Potter. This is in contrast to HFrEF – heart failure with reduced ejection fraction.
From a physiological perspective diastole goes from AV closure to MV closure. It consists of the following phases following AV closure
- IVRT – Iso Volumic Relaxation Time. Where the muscle is relaxing but the volume as yet remains unchanged
- Early diastolic filing – when the MV pops open and the suction effect of the relaxing LV pulls blood from the LA into the LV.
- Diastasis – where the nothing really happens and they all pop out for a quick smoke
- Atrial contraction – the atria gives its puny little ‘kick’ as an attempt to justify its musculature
- MV closure
While we talk about diastole as cardiac relaxation it is actually an active and passive process. Active relaxation begins towards the end of systole continues until end of early filling. Late filling (from end of e wave to end of a wave) is largely passive.
From our point of view we’re looking for it in patients who look like they’ve got heart failure but maybe don’t have an obvious history of it or the cardiac PoCUS looks fairly normal. We should think of it more in
- Older patients
- Those with certain echo signs such as raised right sided pressures, big left atria and things like abnormal E/e’ (which sadly have nothing to do with optimus prime)(of note I misspoke on the audio here and talked about a high e’ being the problem – soz…)
Typically the diagnosis is made with echo and there is a comprehensive guideline document endorsed by the American and European echo societies with lead author Nagueh from 2016 but increasingly it seems that many of the numbers and criteria in that document may not transfer well to the critical care population.
This has relevance to the ICU population in 2 major ares
- EF does not correlate with particularly well with mortality in sepsis though diastolic dysfunction does
- It may be due to under filling and the reduced diastolic filling due to the ubiquitous tachycardia in sepsis. This raises the tantalising possibility of beta blocking the patient on 40mcg/min of norad which as yet can only be described as physiologically interesting but unsupported
- fluid resus here is very tricky as too little bad and too much is bad with no room for error
- Weaning failure
- cardiac is a common cause of failure at extubation. You pull the tube, lose afterload reducing effect of the PEEP and your patient gets reintubated with pulmonary oedema.
- it seems that B lines and filling pressure estimations with echo are more predictive of failure than systolic dysfunction or diaphragmatic dysfunction on ultrasound
This is all very interesting but we are left with the typical conundrum that advancing the understanding of a particular disease process often brings about – we have no proven treatments.
Beta blockers and BP control remain important in the OP population but it is difficult to know how they apply to the ventilated septic ICU patient. From physiological reasoning it may be wise to
- maintain sinus rhythm
- maintain a normal preload
- a low afterload
- and a slowish rate
References and justifications: