I gave my third board review class for the graduating residents at Providence. They requested RTAs. Here are the supporting materials:
Good luck.
What’s new in Potassium: sudden cardiac death
As the Nephrology Fellow Network recently covered the etiology of cardiovascular disease in dialyzors is unique from the general public. Use of statins, the foundation of preventative cardiology, has repeatedly failed to prevent cardiovascular vascular disease (CVD) among dialyzors. One reason for this, is the propensity for these patients to die of sudden cardiac death (a lethal heart rhythm requiring a shock of electricity or luck to reverse) rather than acute myocardial infarction (heart attacks). In this study (PDF), from Italy, the investigators found that nearly half of the cardiovascular deaths were due to sudden cardiac death (SCD). The authors retrospectively looked at their data to find risk factors for SCD.
They prospectively looked at 476 patients in 5 Italian hemodialysis units. The cohort was tracked for 3 years and had 167 deaths (35%), 32 due to SCD and 35 due to other CVD. On multivariate analysis they found the following risk factors for SCD:
As important as what was significant, is what was not significant. Left ventricular hypertrophy, heart failure and valvular heart disease, all important risk factors for SCD among non-dialysis patients were not associated with SCD in their cohort.
The most interesting analysis was when they parsed out the day of the week the patients died of SCD. Instead of looking at the absolute day they related the day to the patients dialysis schedule. I have modifed their chart to reflect this, with twin X-axis: one for MWF and another for TTS patients.
The red line indicates how high the bars would be if there was no relationship to the dialysis schedule. The highest risk periods were the 24 hours before dialysis at the beginning of the week and the 24 hours after the dialysis at the beginning of the week. Not dialyzing for the two days over the week-end put patients at risk for SCD both before and after subsequent dialysis.
This sounds like an electrolyte associated complication rather than a uremic toxin because of the risk after dialysis, indicating the change in the toxin, not just the high level, is a risk-factor. This is supported by studies (1, 2) of potassium modeling in which the potassium in the dialysate is lowered sequentially during dialysis. By modeling the potassium, the speed of potassium removal is decreased. This has been shown to decrease pre-mature ventricular contractions (a benign momentary disturbance in the heart rhythm that is being used as a proxy for more serious arhythmias, like SCD. Medicine has gotten in trouble with this proxy in the past so it may not be appropriate.).
Summary: modestly high potassiums are associated increased SCD and the two day dialysis holiday on traditional three day a week dialysis is likewise associated with SCD. Hello daily dialysis!
The lecture on Potassium that this entry was drawn from:
Whats New In Potassium
View more presentations from Joel Topf.
What’s new with hyperkalemia: EKG changes
Today I did a lecture for the fellows on hyperkalemia. It is interesting that nearly none of the content I use to teach the residents and students is used in a lecture for the fellows. Same subject complete rewrite.
I plan on doing four posts on hyperkalemia from this lecture:
- EKG changes
- Dialysis patients and hyperkalema
- Digoxen toxicity and hyperkalemia
- Renal adaptation to ACEi and aldo antagonists in CKD
The lecture started off with the case I blogged about last week with the scary EKG and the potassium of 9.9.
I focused on a well done study (Full Text) by Drs Montague, Ouellette and Buller from Yale. They looked at 90 patients with a potassium grreater than 6 and an EKG done within an hour of the potassium. They excluded hemolyzed specimens and patients with cardiac pacing or other conditions which would mask EKG changes.
They graded all the EKGs according to a prospective criteria and recorded the cardiologists assessment.
The average patient was 73 years old (20-93) and half had acute kidney injury (55%) and half had chronic kidney disease (47%). They did not comment on the degree of overlap between those groups. Half the patients had diabetes (55%). Only 31% were on ACEi and 30% on loop diuretics.
The reading cardiologist documented peaked T waves in only 3 of 90 patients with hyperkalemia. The investigators were able to find peaked T waves in only 29. QRS widening was found in only 6 patients. Of the 52 patients who could have been classified as having “Strict Criteria” (you needed a second EKG after resolution of the hyperkalemia and not everyone in the cohort had a second EKG) only 16 actually met strict criteria.
The authors found EKG criteria to be insensitive predictors of hyperkalemia:
- Sensitivity of strict criteria: 18%
- Sensitivity of any EKG change 52%
Interestingly, they found that acidosis decreased the likelihood of finding peaked T-waves.
When they looked at arrhythmias as an outcome, EKG changes continued to be a poor clinical guide. They were not sensitive: only one of the patients who subsequently developed an arrhythmia or cardiac arrest had previously met the strict criteria for EKG changes and only 7 had any T-wave findings at all. This is important because it emphasizes the fact that you can not be reassured by a normal EKG in a patient with hyperkalemia.
The study was unable to look at specificity because all of the patients had hyperkalemia. An earlier study by Wrenn, Slovis and Slovis was able to look at sensitivity and specificity because they did have patients without hyperkalemia in their cohort. They retrospectively reviewed the EKGs of 220 patients with either renal failure (n=133) or hyperkalemia (n=87):
- Sensitivity: 39%
- Specificity: 85%
When they restricted the cohort to patients with a potassium over 6.5 the sensitivity rose to 58%.
Take home message: a normal EKG should not rule out hyperkalemia and should not decerase your concearn for impending arrhythmia.
Here is the lecture this post is based on:
Whats New In Potassium
View more presentations from Joel Topf.
Fluid and Electrolyte lecture at Providence from Friday
Third in the series of interesting fluid and electrolyte cases.
I would add a slide on where I was going in potassium before the anorexia section.
SlideSpace botches the torn paper frames I used through out the lecture so if you have Keynote, download and look at the native file.
Here is a link to the Keynote file.
Student lecture on Acid-Base
I gave a lecture to the third-year medical students at Providence hospital on Friday. I thought the lecture went well but on saturday I was going over an admit note by one of the students in the class. The patient was admitted with DKA but had a combined metabolic acidosis and respiratory alkalosis. This student didn’t do the Winter’s formula calculation and missed the respiratory disease. Of course so did everyone else on the admitting team.
Frustrating.
Here is the handout. I added a couple of things since giving the lecture on Friday.
Update: I corrected a mistake in one of the delta bicarb questions. Sorry.
Lecture at Providence Hospital on Electrolytes
I am trying to do a monthly lecture for the Providence internal medicine residents on electrolytes. I gave my second one last Friday. It was an interesting case we had of hypernatremia on the consult service last summer.
I did this lecture in Keynote and I am blown away by how good it presents through SlideShare. Really impressive.
Hypernatremia Hypercalcemia Case Vignette
View more presentations or upload your own.
Fluid and Electrolyte lecture at Providence from Tuesday Dec 16
I did a lecture at Providence last week.
I was scheduled to just give a electrolyte lecture without any further guidance. I pulled out two interesting cases I had seen in the last few weeks. Both patients have a non-anion gap metabolic acidosis, but one is hypokalemic and the other is hyperkalemic.
Here is the native Powerpoint files for you to use or edit.
Here is the SlideShare for online viewing
Acid-Base lecture for ER residents
Yesterday I gave a great lecture on interpreting ABG results. I added a problems set for gap-gap analysis and added a section on the osmolar gap. I also improved the anion gap section with my new favorite nemonic. Forget PLUMSEEDS, forget MUDSLEEPS, forget MUDPILES. The new hotness is GOLD MARK:
- G Glycols
- O 5-Oxoproline (pyroglutamic acid)
- L L-Lactic acid
- D D-Lactic acid
- M Methanol
- A Aspirin
- R Renal failure
- K Ketoacidosis
This new nemonic was published in a letter in the Lancet (thanks vincent bourquin). I love that it drops the silliness of paraldehyde that no one uses anymore and drops isoniazid and iron which hardly ever cause an anion gap.
I also stumbled across a cool article on the sensitivity of the anion gap for lactic acidosis. Surprisingly an anion gap is only found in 58% of patients with an anion gap.
Additionally I cleaned up a bunch of the lecture. I still have not reformatted it for the iPhone so the handout is traditional 8.5×11 without a booklet form.
Sodium and Potassium for ER residents
Yesterday I lectured the St John ER residency program. The ER residency has an impressive commitment to education. They set aside a half day every wednesday for their resident to get dedicated didactic time. They have great attendance with a good number of attendings showing up.
I have been asked to give three lectures and yesterday was the first. I gave a double lecture (running time about 90 minutes) on sodium and potassium. The fact that I could run over the standard 50 minute alotment normally given for medicial education is due to the fact that they have blocked an entire afternoon rather than try to shoehorn a lecture into lunch or before rounds.
The sodium lecture was the first time I used the Sodium handout I created for the St John IM residents. I gave the lectuer Seder-Style with the residents reading different sections, answering questions and me adding commentary. The ER residents are smart and empowered to ask questions. I felt that there was great two-way interactivity.
Sodium iPhone format
Sodium booklet format
The potassium lectuer is an abrdged potassium lecture which is stripped to the bare bones of differential and treatment. It is a traditional powerpoint lecture. Immediately when I started this lectuer I saw about half a dozen exhausted interns fall asleep. My next project is to create a potassium haggadah.
The Acid-Base lecture for the residents of St John Hospital
Today I gave my second lecture of the year for the St John Residency.
I used my Acid-Base workshop handout and added a slide show to facilitate the large group.
I still called on individual residents to answer questions to keep them involved.
I started the lecture with some audience participation. My previous lecture on IV Fluids, diuretics and dysnatremias began with me stating how ubiquitous these subjects were.
I had everyone stand then I asked people to sit down if, in the last three weeks they had not:
- Used any diuretics: no one sat down
- Used any IV diuretics: about half a dozen people sat down
- Used a thiazide diuretic to counter the effect of loop diuretic resistance: lost a lot of people there but still had about a dozen left
- Used a lasix drip to counter loop diuretic resistance from heart failure: everybody sat down but about 3 residents and the amazing Dr. Dhungel, my first year fellow on the consult service.
- Used torsemide instead of furosemide for better pharmacokinetics: only Dr Dhungel remained standing.
I then tried to repeat the excercise for IV fluids and dysnatremias but it didn’t work very well. Should have quit after the first one.
When I gave that IV Fluids, diuretics and dysnatremias lecture I didn’t have a hand out. In the last three weeks I have worked up a handout: