Common+Serum+Chemistries


 * Albumin || 3.5-4.8 gm/dl ||
 * Bicarbonate || 23-28 mEq/L ||
 * Blood Gases (Arterial, Whole Blood) ||  ||
 * pH || 7.35-7.45 ||
 * pO2 || 80-105mmHg ||
 * pCO2 || 34-45 mmHg ||
 * Calcium ||  ||
 * Total || 9.0-10.3mg/dL ||
 * Free || 4.5-5.0 mg/dL ||
 * Carbon Dioxide (Bicarbonate) || 24-32 mEq/L ||
 * Chloride || 95-105 mEq ||
 * Cholesterol || 1-239 mg/dL ||
 * Creatinine ||  ||
 * Male || 0.8-1.3 mg/dL ||
 * Female || 0.6-1.1 mg /dL ||
 * Glucose (fasting) || 65-110 mg/dL ||
 * Magnesium || 1.7-2.7 mg/dL ||
 * Osmolality || 280-290 mOsm/kg ||
 * Phosphorus || 2.5-4.5 mg/L ||
 * Potassium || 3.5-4.5 mEq/L ||
 * Protein (total) || 6.5-8.5gm/dl ||
 * Sodium || 135-145 mEq/L ||
 * BUN || 8-25 mg/dL ||
 * Magnesium || 1.7-2.7 mg/dL ||
 * Osmolality || 280-290 mOsm/kg ||
 * Phosphorus || 2.5-4.5 mg/L ||
 * Potassium || 3.5-4.5 mEq/L ||
 * Protein (total) || 6.5-8.5gm/dl ||
 * Sodium || 135-145 mEq/L ||
 * BUN || 8-25 mg/dL ||
 * Protein (total) || 6.5-8.5gm/dl ||
 * Sodium || 135-145 mEq/L ||
 * BUN || 8-25 mg/dL ||
 * Sodium || 135-145 mEq/L ||
 * BUN || 8-25 mg/dL ||
 * BUN || 8-25 mg/dL ||

Urine SG normal is 1.01 =Case 1= How do know volume overload: edema, weight gain

osmolarity isn't as low as might expect glucose is normal other things: lipid, protein content of serum
 * main thing that affects sodium**

osmolarity is below normal but not by all that much why not lower? High BUN BUN is another small solute contributes to osmolarity to correct, divide by 2.8 incorporates correction for units gives estimate of contribution since BUN is freely passably, does not contribute to water shifts (No tonicity)

calculate osmolar gap: sodiu times 2 + X + BUN times 2.8

osmolar gap does not specify hyponatremia, but can be used to look for small molecule...alchohols ethylene glycol, methanol

if he were hypoglycemic, would have osmolar gap? No, glucose is measured

Are his kidneys responding to clear a free water load? if kidney were 200 mOsm, would imply kidney were working non-osmotic stimulus to ADH is inappropriate? no. has reason for it high intravascular volume behind left ventricle low intravascular volume where baroreceptors are that control adh secretion most situations not maximally dilute if overwhelm w/ polydipsia...could have maximally dilute urine, hyponatremic not as severely hyponatremic as would get in these capacity to clear water s so high

is pt in sodium-retaining state? yes still lots of sodium in system low urine sodium

on thiazide could have interfered but didn't urine sodium is important in distinguishing between hyponatremic states this is hypervolemic hyponatremia

what is cutoff for normal vs low? 20-25 for someone with good renal function lower cutoff in acute renal failure...10-20 or 25...depending on situation of kidney

Total body fluid up low sodium what are other two big categories that do this? 3 big conditions... Hepatic Cirrhosis increases portal venous pressure causing portal HTN, ascites also move fluid out of intravascular space because hypovolemic Nephrotic Syndrome causes lower oncotic pressure What is basis for for pts hyponatremia? Low Cardiac Output Are there any drugs that could have contributed? Thiazide diuretics hyponatremia not a primary problem of sodium, but of water effect of diuretic on sodium concentration is determined by effecton water handling, not sodium handling thiazide limit diluting capability, thus flush sodium

loop diuretics alter thick ascending limb this limits concentrating capability

What hormones contribute? SIADH renin/angiotensin aldosterone

What is best treatment? Loop diuretic? get rid of water. what's causing problem? most effective way is to address heart failure vasodilator resolution of hyponatremia will follow predictably from improvement of cardiac output
 * heart failure**

Should use and monitoring of any current medications be changed? different diuretic or ACEi

=Case 2= What occurred to pt volume? left ventricular disfunction total volume body status is fine or low other clues: low urine sodium, high concentration of urine normal, or low could be left ventricular output w/ decreased kidney function How would treatment differ from that of pt A? no diuretics

pulmonary artery... PCWP... Both but only A has increased central venous pressure

=Case III= 45yo male in ED with weakness, nausea, vomiting alchohol heavily 1 week until 24 hr earlier decreased dietary intake BP 110/70 HR 110 rr 30 temperature 102F seizure Na 137/ K 2.8 CL 86 Bicarb 37 pCO2 33 pH 7.67 Mg 0.8 Ca 7.0 alumin 3.6 glucose 60

redistribution? of potassium? Alkalemic Fever... drives epinephrine intake decreased obligatory vomiting causes redistribution... favors potassium excretion in kidney volume depletion if administer 5% dextrose.... potassium will go down

Bolus of glucose... 5% dextrose d5W graded amount not a bolus Why would decreased glucose pull potassium out of cells? whenever pull water out of cells, will concentrate potassium

pCO2 is low.....so also respiratory alkalosis

What would urine chloride be? Low........ volume depleted serum chloride is low urine chloride used because urine sodium can be disleading bicarbonate pulls sodium with it

what should give him? sodium chloride depleted... chloride responsive vs chloride unresponsive replacing chloride is central to correction

for every 0.27 need 100s of mEq may also need magnesium seizures...hyperexcitable state Do we need to give glucose? yes,but also ned to give thymine otherwise give wernicke's encephalopathy

=Case IV= 63 YO prviously non-insulin dependent diabetic has been experienceing increasing poluria, polydipsia several weeks finger stick glucose 500 checking BP at home.... picked up salt substitute at krogers.... HTN

contrived case? no.

anything giving pseudohyperkalemia? hemolysis one factor...diabetes non-insulin dependent beta-blocker causing redistribution basement membrane? Ace Inhibitors cause hyperkalemia by inhibiting aldosterone effects, but do not cause redistribution

acidosis? what about the kidney problem? low GFR

anion gap-23

what else is needed? EKG

brief sodium channels get shut off sustained excitability in hyperkalemia is suppression of excitability calcium is restoring that also works via calmodulin What are other ealry maneuvers? does calcium do anything to serum potassium?

loop diuretic 'make them pee more'

aldosterone? takes time

insulin redistribution

dialysis kayexalate

sacricie beta blocker before sacrificing ACEi water balance is not normal

she has a water deficit hypernatremic