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Introducing the Acid-Base Machine

Last month I realized that in order for students to really learn acid-base interpretation they need practice. Lots of practice. So I started everyday’s teaching rounds by assigning each student four ABGs to interpret.

Creating all of those ABGs became pretty tedious so I started fiddling around with an excel spreadsheet to automate the process. I used ABG Machine 1.0 for that month but, unfortunately, it created too many respiratory problems and too few metabolic disorders. I completely re-crafted the randomization algorithm so that it should provide a balanced distribution of ABG problems (a quarter metabolic acidosis, a quarter metabolic alkalosis, a quarter respiratory alkalosis and a quarter respiratory acidosis).

Introducing The Acid-Base Machine 2.0

The spreadsheet is made up of 12 individual sheets. The first one is the Question sheet, you should print one copy for every student or resident. The second sheet is the Answer sheet, I printed one for me and one for each student and I would pass them out after the excercise so if they wanted to brush up on some additional questions they had the answers. The next ten sheets are the guts of the machine and you can ignore them unless you want to tinker with how the randomization works.

Download the Excel file

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Is hypertension in octagenarians a characteristic or a disease

I was at the NKF Spring Clinical meeting and I saw variations of the two following slides in at least three different lectures:

The slide on the left comes from the AHA Heart Disease and Stroke Statistics from 2007 (PDF). It shows the increasing prevalence of hypertension as people get older. The slide on the right is from the Framingham Heart Study (PDF) and shows the 20 year risk for normotensive adults for developing hypertension. Both figures are repeated below:


The part of these figures that kept gnawing at my brain was putting them together, stacking them if you will. 60-70% of the sixty-year olds have hypertension and the minority that are normotensive have a 90% chance of developing hypertension by the time they are 85. So essentially every 80 year old has hypertension.

Does hypertension cease to be a disease when everybody has it? Is hypertension less pathology and rather part of the normal physiology of aging?

Speaking against the idea of geriatric hypertension being normal physiology is the powerful survival advantage gained by treating the high blood pressure. This data comes from HYVET published last spring in the NEJM (PDF). Prior to HYVET there was retrospective data pointing to better survival with higher blood pressures (Oates 2007) and a meta-analysis of 80+ year olds enrolled in RCTs showed a reduction in cardiovascular evens but a trend to increased total mortality.

The HYVET ransdomized 3,845 octagenarians with blood pressures 160-190 with a diastolic of less than 110 to either placebo or indapamide (thiazide-like diuretic) with additional perindopril if the systolic blood pressure remained over 150. The primary end-point was number of strokes (fatal + non-fatal)

Results. The investigators achieved good blood pressure separation between the control and experimental groups with a 15 mmHg difference in the systolics and 6 mmHg difference between the diastolics.

The effect on morbidity and mortality were dramatic (all results expressed as intension-to-treat) with active treament resulting in:

  • 30% reduction in the rate of fatal or nonfatal stroke (95% confidence interval [CI], –1 to 51; P=0.06)
  • 39% reduction in the rate of death from stroke (95% CI, 1 to 62; P=0.05)
  • 21% reduction in the rate of death from any cause (95% CI, 4 to 35; P=0.02)
  • 23% reduction in the rate of death from cardiovascular causes (95% CI, –1 to 40; P=0.06)
  • 64% reduction in the rate of heart failure (95% CI, 42 to 78; P<0.001)
  • Fewer serious adverse events (358, vs. 448 in the placebo group; P=0.001).
Click on the graphs to see larger versions.

So even if hypertension in the elderly is not a disease, treating it seems to have dramatic benefits for patients. Vote your opinion!

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Its not the sodium intake its the sodium:potassium ratio

Don’t worry only about sodium intake (NYC, I’m looking at you) and its not just potassium intake (DASH diet in the cross-hairs). It’s all about the sodium potassium ratio. This is shown by Cook et al (PDF). during reanalysis of the Trial of Hypertension Prevention I and II. This trial had serial 24-hour urine collections done in 2,275 patients with pre-hypertension in the late 80’s and 90’s. The investigators looked at that data through the lens of 15 years of follow-up to determine the risk of cadiovascular events:

In observational analyses of the mean urinary excretion during 11⁄2 to 3 years, we found a suggested positive relationship of urinary sodium excretion and a suggested inverse relationship of urinary potassium excretion with risk of CVD, but neither was statistically significant when considered separately. Both measures strengthened when modeled jointly, with opposite but similar effects on risk. However, the sodium to potassium excretion ratio displayed the strongest and statistically significant association, with a 24% increase in risk per unit of the ratio that was similar for CHD and stroke and was consistent across subgroups.

Here is the key figure. Note in the graph the rate of events is presented on a log scale so the 2 indicates a rate 100 times the rate at zero.

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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: