Magnesium
                                   =========

þ Magnesium avidly retained by kidney; absorbed in small intestine.
  Like Ca++, is very much protein bound.  Stored in bone.

þ MgCl2 is most easily absorbed.  Enteric-coated versions decrease GI
  intolerance.  Green vegetables have high Mg++.

þ Increased requirements from western diet (EtOH, fat), stress, catecholamines)
  "10 D's" that increase Mg++ requirements:
 - diarrhea
 - diet (fat)
 - drinking (EtOH)
 - D (vitamin D)
 - diuretics
 - decreasing renal function with age
 - dealing with stress (catecholamines)
 - delivery and pregnancy, toxemia.
 - diet (phosphorus)
 - diet (calcium)

þ Only 1% in serum; serum values not very useful; muscle Mg++ best.
  No correlation between serum Mg++ and Mg retention when loaded with Mg++ and
  urinary excretion measured; this is another reasonable test.

þ Mg++ deficiency leads to K+ deficiency, because kindey needs Mg++ to reabsorb
  K++

þ Mg++ and cardiac cells; important cofactor in Na+/K+ ATPase; affects Ca++
  metabolism

þ Mg++ and EKG:  deficiency is like hyperkalemia; peaked T-waves, QRS flattening
  in later stages. Giving Mg++ will prolong QRS and PR and refractory period in
  atria and AV node, but not in His bundle or venticular Purkinje system;
  doesn't affect QT interval, SA node, heart rate.  In deficiency, ATPase
  doesn't work, so serum K+ rises near cells.  (Rasmussen HS, et al. The
  electrophysiological effects of IV Mg on human sinus node, AV node, atrium,
  and ventricles. Clin Cardiol 1989;12:85-90)

þ Mg++ supplementation has cardioprotective effect; higher incidence of sudden
  death in areas with Mg++-deficient soil; Mg deficiency also predisposes to
  coronary spasm.  (Anderson TW, et al. Sudden death and ischemic heart disease
  correlation with hardness of local water supply. N Engl J Med 1969;280:805-7.)

þ Mg++ reduces serious arrhythmias (VT, VF, Triplets, R on T) is 24 hours post
  MI*, (6 g IV over 3 hours then 10g/24 hours decreased mortality even more than
  accounted for by arrhythmia decrease).**  (They may all be Mg++ deficient.)

þ Mg++ and CHF:  diuretics cause Mg++ wasting as well as K+ wasting; increased
  aldosterone increases Mg++ loses; CHF'ers may have poor GI absorbtion
  ("Cardiac Cachexia").

þ Mg++ and digitalis toxicity: first report in 1935.
  2-4g bolus, then constant infusion serum levels of 4-5 mEq

þ Mg++ and Toursades de Pointes***:  2g IV bolus Mg++ in 12 patients, no placebo
  controls, showed good effect; doesn't decrease QT interval, so mechanism not
  known.  9 responded to first 2g, other 3 responded to second bolus.

þ Mg++ and SVT:  7/10 responded with initial bolus, had transient flushing.****
  Mg++ may help with SVT but shouldn't affect ventricular arruythmias

þ Mg++ helped convert some people who were not hypoxic from MAT. Noted that K+
  levels fell after Mg++ administration; supposed this was from L+ entry into
  cells.*****

* Rasmussen HS, et al. Mg deficiency in patients with ischemic heart disease
  with and without MI uncovered by an IV loading test. Arch Int Med
  1988;148:329-332.
** Schecter M, et al. Beneficial effect of MgSO4 in acute MI. Am J Cardiol
   1990;66(3):271.
***Tzivoni D, et al. Treatment of Torsade de Pointes with mg-sulfate.
   Circulation 1988;77:392-7
****Wesley RC, et al. Efect of intravenous mg-sulfate on SVT. Am J Cardiol
    1989;63:1129-31..
*****Iseri LT, et al. Magnesium therapy of cardiac arrhythmias in critical care
     medicine. Magnesium 1989;8:299-306.