Welcome back to the tasty morsels of critical care podcast.
Today we tackle a somewhat nebulous syndrome. Something we throw around with a few hand wavy explanations but often light on detail. Hopefully in a few minutes you’ll at least have a few morsels more of information to stave off all the trainees who are undoubtedly much smarter than you on the ward round. But perhaps I’m getting too autobiographical already.
This does not appear with any great frequency in Oh’s manual but there is a nice scientific statement from the AHA that is referenced below. Though when you call it a statement you imagine some nervous spokesman in front of a camera trying to explain why is boss has done something naughty. Instead this is a 39 page epic review of the topic.
To start with there are apparently 5 types of cardiorenal syndrome. I’ll let that sink in. You all thought there was one didn’t you?
Type 1 is the acute deterioration in kidney function seen in cardiogenic shock from ACS. Type 2 is the slow and chronic deterioration of kidney function in the chronically failing heart.
They get sneaky with type 3 calling it renocardiac syndrome. You see what they did there they just reversed cardiorenal syndrome and called it renocardiac syndrome. In this scenario the kidney has acutely been injured and the consequences such as fluid overload cause heart failure. Type 4 is again renocardiac with the kidneys causing the heart failure but on a chronic basis. With me so far?
Type 5 is the big bucket where they put all the left over disease that cause both kidney and heart failure eg things like amyloid, or sepsis or cirrhosis.
Certainly when i use the term in daily practice i was only ever thinking of types 1 and 2 and that’s what we’re going to focus on in this tasty morsel.
Why does this happen. I’ll paraphrase the opening part of the pathophys section from the scientific statement. Conventionally we focus on poor forward flow from the heart causing poor renal perfusion, poor GFR and activation of the RAAS. But in the style of a telemarketing TV advert “wait there’s more”. Poor forward flow is by no means the only pathology and in fact high pressures on the venous side likely contribute to the phenomenon of cardiorenal syndrome. for example we know that a MAP of 65mmHg is a generic target for perfusion pressure for most organ beds. However the actual calculation of perfusion pressure is probably better represented as MAP-CVP. Therefore in those with CVPs chronically sitting in the 10-15 range, you are going to struggle to effectively perfuse their kidneys. You’ll even here this called congestive renal failure on occasion.
Along the same lines it’s worth thinking about the impact of intrabdominal pressure on renal perfusion, those with tense ascites from heart failure are also going to struggle. There are of course much more complex neurohumoral, inflammatory type cytokiney thingies going on but as you can tell they are well over my head so I’ve skipped them for now.
You might think that diagnosis of cardiorenal syndrome might be straightforward. We just check a creatinine and if it’s high it’s a problem. But there are a fairly bewildering array of tests available for assessing renal function beyond the very blunt stick of creatinine. Things that rejoice in names like NGAL or cystatin C or looking at albuminuria; all may have a role in teasing out CRS from other issues. Valuable as it is for filling the 39 pages of the scientific statement i can’t see any great relevance to the jobbing intensivist. Of note in the paper, and perhaps obscured by the detail of the available biomarkers is the note that fluctuations in creatinine are often poor representations of actual kidney injury. I took home from this discussion that as long as they are still diuresing effectively we shouldn’t be in a rush to hold the diuretics purely because the creatinine bumped.
Of note as part of the diagnostic work up the statement does give a shout out to the much maligned and greatly missed PAC. This might allow us to effectively assess congestion while avoiding the terrors of hypoperfusion from volume removal.
Moving swiftly on to management strategies I think it’s clear that diuretics have a clear role in congested heart failure patients. However there does seem to be a reluctance to give diuretics once the creatinine bumps up anywhere above the normal range. There is a pervasive (and unfounded) belief that loop diuretics are directly nephrotoxic and as such should not be given. But if we’ve been paying attention so far we’ll realise that congestion itself may be causing the kidney injury and decongestion may well fix things. Now of course we need to be a doctor about this and have a think about other causes of AKI beyond simple congestion but for the sake of the podcast we will assume that we have the correct diagnosis.
Let’s say we have done the right thing and given a decent dose of loop diuretic despite the bump in the creatinine, we often encounter something called the “braking phenomenon”. This refers to the idea that we get less and less response to each successive dose of diuretic, and this can develop over hours. The pathophys of this is beyond the scope of this podcast but involves the nephron doing what it does best in a crisis and tries to hold on to more sodium. You can get around this by making a flanking attack on the nephron by bringing in something like a thiazide in addition. Indeed the concept of the Nephron Bomb covered in tasty morsel 68 (first made popular to me by Joel Topf known as kidneyboy on twitter) is a clinically compelling and somewhat entertaining way to approach pharmacology of diuresis.
Of note there comes a certain point where no matter the diuretic stratgey the volume of wee wee produced is insufficient. And this indeed portends a poor prognosis. Ultrafiltration with whatever mode of RRT you choose seems a compelling option but has performed poorly in most trials to date. Either because it simply doesn’t work or possibly because those sick enough to qualify for an ultrafiltration trial have already found themselves in a category of patients likely to do poorly no matter what.
This segues relatively nicely into a section of the document on palliative care. It is important to realise that a referral to ICU for refractory cardiorenal syndrome may simply be a sign that the patient is reaching end of life. Adding an extra machine to a patient at end of life is not good form and it is incumbent upon us to do the work to figure out if we have some degree of reversibility (eg from acute congestion) or if this is just progression of an underlying irreversible disease process
– Rangaswami, J. et al. Cardiorenal Syndrome: Classification, Pathophysiology, Diagnosis, and Treatment Strategies: A Scientific Statement From the American Heart Association. Circulation 139, e840–e878 (2019).
– Mullens, W., Verbrugge, F. H., Nijst, P. & Tang, W. H. W. Renal sodium avidity in heart failure: from pathophysiology to treatment strategies. Eur Heart J 38, 1872–1882 (2017).
– Mullens, W. et al. Evaluation of kidney function throughout the heart failure trajectory – a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail 22, 584–603 (2020).