One hour lecture on NAGMA. Just some small changes edits from the last time I gave it. It is one of the few lectures that is still in PowerPoint. It is due for a complete overhaul. It also needs a slide on the treatment of RTA that covers the amount of bicarbonate in a 650 mg tablet (8 mmol) and the fact that distal (type 1) RTA requires a limited amount of bicarbonate (at most 1 mmol/kg). This is appropriate for residents and medical students.
If you are interested in ward teaching and RTA, take a look at this post by Robert Centor.
Also this is a nice article on the issue of saline having a pH of 5.5, covering both the reason (its the PVC bag) and the implications (none).
I am going to Kings Canyon National Park at the end of the month. I will leave Detroit, elevation 600 feet and will travel via planes, trains and automobiles to 9,000 feet for the first night. Then we will begin out hike and cross passes over 12,500 feet.
In the past, I have developed modest altitude sickness going from 600 to 8,000 feet. So, I am nervous about the same problem on this trip. Acetazolamide is supposed to ameliorate altitude sickness.
The body acclimates to decreased oxygen and is so effective that people can function at the top of Mt. Everest without supplemental oxygen. The partial pressure of oxygen at the summit is 43 mmHg which is equivalent to breathing 6% FiO2.
|From NEJM 2009, 360: 140-9
The primary means of improving oxygenation is hyperventilation. Hypoxia stimulates ventilation. There is also an increased ventilatory response to carbon dioxide so that that the normal respiratory response to carbon dioxide is exaggerated so that one gets more ventilation at lower CO2 levels. The reason that increased ventilation improves oxygenation has to do with the effect carbon dioxide in the blood has on oxygen transfer in the alveoli. During respiration CO2 leaving the blood dilutes the incoming oxygen at the alveoli, increased respiration, lowers the pCO2 and hence minimizes this dilution.
Antagonizing the hyperventilatory response is respiratory alkalosis. Central chemoreceptors detect alkalosis in the CSF and slow respiration. This is one of the key factors preventing the essential hyperventilation.
Acetazolamide (Diamox) is a carbonic anhydrase inhibitor. Carbonic anhydrase catalyzes the reaction converting bicarbonate to carbon diaoxide and water:
This is the fundamental buffer reaction in the body and it is amazing to me that blocking this essential acid-base reaction is not lethal. Acetazolamide works in the proximal tubule by blocking the reabsorption of filtered bicarbonate.
Acetazolamide induces a proximal renal tubular acidosis (RTA 2). This results in metabolic acidosis. The metabolic acidosis stimulates compensatory hyperventilation. This metabolic acidosis antagonizes the respiratory alkalosis which normally occurs with hyperventilation.
Their maybe additional advantages of acetazolamide including decreased CSF production and antagonizing fluid retention.
Hypokalemia can induce rhabdomyolysis. The purported mechanism is that hypokalemia antagonizes one of the natural causes of exercise induced vasodilation. Normally, during exercise muscles release intracellular potassium causing local pockets of hyperkalemia which triggers vasodilation and increases perfusion to the active myocytes. Total body potassium depletion and hypokalemia decrease local hyperkalemia preventing the vasodilation which results in tissue hypoxia and rhabdomyolysis.
In The Fluid and Electrolyte Companion we illustrated it thusly:
I remember thinking how funny it was that we used bowling to represent exercise (though we did slide in those runners behind the bowler). Oh clipart, how much nerdtainment you have given me.
This past week-end one of my patients experienced this. He is a high school student who loves to fish. He has congenital type 2 RTA, so is predisposed to hypokalemia. The exercise that triggered his rhabdo: fishing. He presented to the ER following a day of fishing with complaints of muscle cramps and weakness. His potassium was reported as less than 2, with CPKs in the 800 range.
One of the unexpected consequences of the rhabdomyolysis was that his cramping continued after the potassium was corrected. In fact, it was actually much worse muscle spasm and tetany of the hands. Turns out, this second round of neuromuscular symptoms weren’t due to hypokalemia but rather rhabdomyolysis induced hypocalcemia. He had a normal total calcium and a low ionized calcium. The muscular symptoms responded to a gram of IV calcium gluconate.
I gave my third board review class for the graduating residents at Providence. They requested RTAs. Here are the supporting materials:
- Power point presentation (link)
- Active ABG problem generator (link)
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
I’m running the on-call gauntlet.
I was on call Sat and Sun December 6,7
Sat December 13
Sat and Sun December 20,21
Thursday through Sunday December 25-28
four straight week-ends, with Christmas thrown in for the Jew. Ughh.
That said this week-end has had a few great cases:
- IgM Cold-agglutinin hemolytic anemia in need of plasmapheresis.
- Fluconazole induced hyperkalemia
- Urinary obstruction induced electrogenic type 1 RTA (Hyperkalemic variety of type 1 RTA)
- Primary hyperaldosteronism induced hypertensive emergency
I’ll elaborate on some (all) of these cases in the next few days.