Bold and BRASH
As we all know, one of the cornerstones of nephrology is the intimate relationship between the ever-present and masterfully made kidneys and that other thing less important thing a little higher up that pumps blood (remember this is a nephrology blog.) In all seriousness though, we can never forget that renal disease inevitably begets cardiac disease and vice versa and must always be vigilant about that relationship. And of course, there are many ways that this phenomenon called cardiorenal syndrome comes to exist. I want to touch upon a special phenomenon called BRASH syndrome.
BRASH syndrome which stands for Bradycardia, Renal Failure, AV-nodal blocking agents, Shock, Hyperkalemia is a phenomenon that usually occurs (but not necessarily required) in the setting of AV-nodal blockers that cause bradycardia which leads to poor renal perfusion which progresses to renal failure which causes hyperkalemia which in turn leads to worsening bradycardia and the cycle continues. It is an incredibly interesting scenario in that seemingly unrelated or previously thought unrelated components are very closely related.
Looking back, people have described a phenomenon whereby people who have bradycardia end up in renal failure. Physiologically this makes perfect sense when thinking about cardiac output as seen below:
Cardiac Output = Heart Rate X Stroke Volume
As heart rate drops stroke volume is not always enough to keep up with cardiac output especially if a patient has pre-existing cardiac disease and cannot mount a good volume response to drop in HR. Patient’s with kidney disease are also susceptible to this. Eventually, patients will go into shock from this perpetual cycle.
Treatment for this disease really hinges on two things: restoring sinus rhythm at appropriate which should in turn start to relieve acute kidney injury by restoring renal perfusion and temporizing patients with hyperkalemia. In most cases invasive measures like transvenous pacing are NOT necessary unless advanced heart blocks are present however medications such as dopamine or isoproterenol or even epinephrine can be used to try and restore perfusion to the kidney. If patient’s have suspected AV-nodal blocking agent toxicity even conventional methods like glucagon or insulin drip are not usually necessary. Next, IV calcium should be used to help stabilize cardiac membrane to prevent further bradycardia. Then, kaluresis is important as well to help stop bradycardia. If a patient is hypovolemic fluid resuscitation is very important and Lactated Ringers or Bicarbonate infusion can be used based on the patient’s acid-base status. Also, if patient is anuric, diuretics can be tried to help open up kidneys to eliminate potassium however if patient’s do not respond, dialysis may be required to intervene in this cycle to prevent further bradyarrhythmia and/or arrest.
Overall, BRASH syndrome is a sometimes-overlooked entity which can be resolved quickly if caught early and usually can prevent worsening renal and cardiac disease.
Major Take Away Points:
1) BRASH Syndrome - Bradycardia, Renal Failure, AV-nodal blocking agents, Shock, Hyperkalemia
2) Vicious cycle where one entity (sometimes started by AV-nodal blockers) usually leads to another
3) Occurs due to drop in cardiac output from bradycardia without appropriate response of stroke volume to compensate
4) AKI occurs in low flow state causing renal hypoperfusion leading to pre-renal state and possible ATN causing build-up of potassium
5) Treatment relies on managing bradycardia to restore renal perfusion, and cardiac membrane stabilization along with kaluresis
For more information, there is a great review here:
image courtesy: https://spongebob.fandom.com/wiki/Bold_and_Brash
Rushang Parikh, MD
Rushang Parikh, MD