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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:

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Not nephrology, Passover

I put together a Haggadah and Coloring book for last night’s seder. Enjoy.

By the way, neat nephrology related passover tid bit in Numbers 11:31-33. You can read about it on page 4 of the handout on this page.

The Topf Haggadah 2009 The Topf Haggadah 2009 jtopf6981

Passover Coloring Book 2009

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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:

  1. EKG changes
  2. Dialysis patients and hyperkalema
  3. Digoxen toxicity and hyperkalemia
  4. 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:

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Statins fail again

Statins have a tortured relationship with nephrology. Our patients have accelerated atherosclerosis and they die overwhelmingly of cardiovascular disease. So one of my primary jobs is to continually optimize cardiovascular risk factors to save my patients

Control blood pressure, start an aspirin, and maximize the statin are the lather, rinse, repeat of my world.

That said we have little data that this makes a whit of difference, at least in our dialysis patients.

Aspirin

  • No randomized trials have been done on the role of aspirin to prevent cardiovascular events among dialysis patients.
  • Aspirin was found to increase acute coronary syndrome in an unbadjusted analysis but was not significant in multivariate analysis.
  • Berger et al. (PDF), however found a dramatic reduction in 30-day mortality for patients with acute myocardial infarction given aspirin. Unfortunatly fewer dialysis patients received ASA and other standards of heart-attack care (beta-blocker and ACEi) than patients not on dialysis.
The survival of patients based on whether they received ASA for their acute MIThe use of standard therapies for acute myocardial infarction was lower among dialysis patients, even patients deemed ideal candidates for the therapy.


Blood pressure

  • Hypertension, along with cholesterol and obesity, is subject to reverse epidemiology in dialysis patients. This means that observed epidemiology trends are the opposite of what you would expect from data on non-dialysis patients. Lower blood pressure leads to high mortality, lower cholesterol leads to higher mortality, increased BMI yields better observed survival. The observational data, however, does not mean that interventions to lower blood pressure will lead to the same bad outcomes.
  • A recent meta-analysis (PDF) of 8 randomized trials of anti-hypertensive therapy gives credence to the practice of treating hypertension in dialysis patients.

  • One thing high lighted by the trial, though, is the paucity of evidence for this treatment: They were able to find only 1,679 patients. Terrible.

Statins

  • The 4D study is one of the few randomized controlled trials in dialysis patients and unfortunately did not show any improvement in mortality with atorvastatin. The study randomized 1,255 hemodialysis patients to either 20 mg of atorvastatin or placebo. After 4 years they found the statin was safe and effective in reducing the median serum LDL cholesterol level by 42%. However, the primary endpoint—cardiac death, nonfatal MI, and stroke—was reduced by insignificant 8% (P=0.37).

  • The authors found a significant increase in fatal strokes among the patients randomized to atorvastatin. (RR 2.03, P=0.04).
  • Today came word that another randomized controlled trial on statins among hemodialysis patients, AURORA, was also a bust. Published yesterday in The Journal, AURORA randomized 2,776 dialysis patients to 10 mg of rosuvastatin (Crestor) or matching placebo. The end-point was a composite of CV death, non-fatal MI, and non-fatal stroke. Average follow-up was 3.8 years and there was no difference in the primary outcome (396 outcomes with rosuvastatin versus 408 on placebo, P=0.51).

  • AURORA found no increased risk of strokes as found in the 4D study.
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EKG Changes with hyperkalemia

Last week one of our second-year fellows was called into the ER for a potassium of 9.9 mEq/L. The EKG you see above was waiting for him. He arranged for emergent dialysis. In the morning the patients EKG looked like this:

Here is the time line of events:

  • 17:24 Na 128, HCO3 9, Cl 103, BUN 100, Cr 5.6 (no potassium was reported out on the initial labs)
  • 18:06 First EKG done
  • 18:28: K=9.9
  • 18:28: U/A Sp Grav 1.012, pH 5, random drug screen positive for opioids
  • 18:45: ABG 7.05/37/408/10
  • 18:45: urine Na 89, urine Cr 50.5, FENa 4.7%
  • 23:00 initiate dialysis: 2 hours on 1 K bath
  • 01:00 complete dialysis
  • 03:30 Na 140, K 5, Cl 107, HCO3 16, BUN 67, Cr 3.8, Ca 9.1, Phos 6.4, Mg 1.4, CPK 941
  • 03:30 ABG 7.22/40/117
  • 09:20 Na 142, K 4.8, Cl 111, HCO3 15, BUN 63, Cr 3.2
  • 10:00 ABG 7.20/42/96

This patient had AKI due to prolonged decreased po intake along with a loop diuretic and ACEi. The patient initially was anuric but rapidly began to recover and by the next morning was making over 100 mL of urine an hour.

His initial EKG is the best example of a sine wave from hyperkalemia I have ever seen. Below is a cardiac cycle from V4. With a quick glance it may look like a very wide QRS complex with the t wave somewhere to the right of the picture. In reality, the QRS duration is only 176 msec and the large upward thrust is the peaked T wave.


EKG Changes with hyperkalemia

  • Peaked T waves
  • Shortened QT interval
  • Widened QRS
  • Sine wave
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Great article on the two new PSA studies in the NEJM

The New York Times has good coverage of the latest data (US Study, European study) on prostate cancer.

I loved this beat which covers the difference between relative and absolute risk and NNT:

[After discussing the 20% reduction in mortality found in the European study] But in terms of individual risk, even that is not a huge benefit. It means that a man who isn’t screened has about a 3 percent average risk of dying from prostate cancer. If that man undergoes annual P.S.A. screenings, his risk drops to about 2.4 percent.

And there is an important tradeoff. P.S.A. testing increases a man’s risk of being treated for a cancer that would never have harmed him in the first place. The European study found that for every man who was helped by P.S.A. screening, at least 48 received unnecessary treatment that increased risk for impotency and incontinence. Dr. Otis Brawley, chief medical officer of the American Cancer Society, summed up the European data this way: “The test is about 50 times more likely to ruin your life than it is to save your life.”

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William Schwartz, the co-discoverer of SIADH has died

William Schwartz has died.

Every Monday at noon during fellowship we had the fluid and electrolyte conference with Dr. Fred Coe. Dr. Coe has extra-sensory powers for electrolytes. When you presented, you would give just the electrolytes and he would re-create the entire case from the metabolic panel. During the lecture he would ask you to explain a certain pathophysiology and then excoriate you if your thoughts were lazy and poorly organized.

If you ever blamed a poorly characterized hyponatremia on SIADH, Dr. Coe would look at you and ask “If Bartter and Schwartz were here, at this table, right now, and were looking at the same data that you have provided, would they agree that this is SIADH? Would they?”

JASN re-printed the original 1957 article describing SIADH in 2001.

Goodbye Dr. Schwartz, yours are the shoulders we stand-on in the daily grind of clinical nephrology.