will see flattened T waves and U waves on ekg
RTAs 1 and 2, worry if <2.5. Can lead to rhabdomyolysis
GI losses, ampho B, Insulin, Rta, Diet, Burns, Alkalosis, Timentin and other pcns, Hypomagnesaemia, Steroids. Diuretics, Cushing’s, Familial Periodic Paralysis, Hyperthyroidism
Need ~40 mEq of K to increase 1 mEq/L
A patient who is hypokalemic in the face of ACIDOSIS and is getting insulin to boot, may be another exception. Acidosis shifts K from the cell to the extracellular compartment. Serum K tends to rise. a K of 2.5 may be equivalent to a K of 1.5 in a patient with normal pH. The insulin will further drop his serum K. Yes, I would give KCl in this setting. The danger is giving potassium to a patient in ALKALOSIS where the observed hypokalemia is an effect of the pH. The most common setting for hyperkalemic arrest is in patients who are on chronic diuretics, have chronic mild hypokalemia because of chronic depletion, and their intracellular potassium is also low. The also have contraction alkalosis, and because the K gets artificially very low, are getting aggressive (20 mmol/h) K replacement. These patients may arrest at K levels of 5-6. and as their alkalosis is corrected may get there pretty darn quick. Your patient is the exact opposite example, and his hypokalemia should have been corrected. I never argued that one should never correct hypokalemia. In most cases, however, it should be corrected slowly, preferrably with oral potassium.
Hypokalemia!Pearls to keep in mind:
- When treating significant hypokalemia with IV potassium replacement, initial therapy should consist of potassium administered in glucose-free solutions. Glucose may cause a further decrease in the serum potassium concentration, presumably caused by the enhanced insulin secretion stimulated by glucose, which results in the movement of potassium into cells. This has been documented to precipitate arrhythmias and neuromuscular paralysis (1,2).
- Magnesium depletion often coexists with potassium depletion as a result of drugs (e.g., diuretics) or disease processes (e.g. diarrhea) that cause loss of both ions. Magnesium depletion reduces intracellular potassium concentration due to impairment of the activity of cell-membrane NA+/K+-ATPase and causes renal potassium wasting. Regardless of the cause, the ability to correct potassium deficiency is impaired when magnesium deficiency is present, particularly when the serum magnesium concentration is < 0.5 mmol/L. Magnesium repletion improves the coexistent potassium deficit (1,3).
- The reduction in serum potassium allows only a rough approximation of whole body losses. On average, serum potassium decreases by 0.3 meq/L for each 100 meq of potassium reduction in total-body stores, but the response is extremely variable (1).
- According to the most recent AHA/ACC guidelines it is “reasonable” to maintain serum potassium > 4.0 meq/L in patients with an acute MI (3).
- Severe potassium depletion (< 2.5 meq/L) can lead to rhabdomyolysis (2,4,5). Potassium release from muscle cells normally mediates vasodilation and increased blood flow to muscles during exercise. Decreased potassium release due to profound hypokalemia may diminish blood flow to muscles in response to exertion.
- Potassium repletion is most easily done orally. The serum potassium concentration can rise acutely by as much as 1-1.5 meq/L after an oral dose of 40-60 meq, and by 2.5-3.5 meq/L after 135-160 meq (6). These effects, however, are often transient as much of the exogenous potassium will be taken up by the cells.
References: (1) Agarwal A, Wingo CS. Treatment of hypokalemia N Engl J Med 1999;340: 154-5. (2) Gennari FJ. Hypokalemia N Engl J Med 1998;339:451-458. (3) Zipes DP, et al. American College of Cardiology/American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines Circulation 2006;114:1088-1132. (4) Shintani, S, et al. Marked hypokalemic rhabdomyolysis with myoglobinuria due to diuretic treatment Eur Neurol 1991; 31:396. (5) Dominic, JA, et al. Primary aldosteronism presenting as myoglobinuric acute renal failure Arch Intern Med 1978;138:1433. (6) Nicolis, GL, et al. Glucose-induced hyperkalemia in diabetic subjects Arch Intern Med 1981;141:49.
cardiac abnormalities are common when > 6.5
not a stepwise progression, can go from none to fatal dysrhythmia (J of Crit Care 2008;28:431)
Renal insufficiency, adrenal or aldosterone insufficiency, diuretics or ACEI, Type IV RTA, Tumor lysis or Rhabdo, Hemolysis, GI Bleeds, Pen-VK, DKA, Beta Blockers, Digoxin Overdose,
Drug Dose Onset DurationCalcium Chloride 500-1000 mg 1-3 Min 30-60 min Sodium Bicarb 150 meq in 1 liter fluids run like IV fluids variable variable Insulin/Glucose 10 units Insulin/50 g D50 then add 20 units RI in 1 liter fluids with 2 amps D50 added run over 2 hours 30 min 4 to 6 hours Albuterol 10-20 mg over 15 min 15 min 15 to 90 min Furosemide 40 -80 mg c diuresis until end of diuresis Kayexylate 15-50 g (PO or PR) plus sorbitol. For enema: 50 g mixed with 50 cc of 70% sorbitol plus 100 cc tap water 1-2 hours 4-6 hours
Calcium: use chloride in code/shock as gluconate requires hepatic conversion
Insulin/Glucose-20 u and 25 g in 100 cc d5w give over 10 minutes
Albuterol-10 to 20 mg
Bicarb-1 mEq per kg in acidotic pts
Box 1: Causes of pseudohyperkalaemia
- Related to collectionand storage of specimen:
- Difficulty in collecting sample
- Patientclenched fist when sample was taken
- Sample was shaken or squirtedthrough needle into collection tube
- Contamination with anticoagulantfrom another sample (potassium EDTA)
- Deteriorationof specimen due to length of storage
- Pre-existing conditions:
- Severeleucocytosis (which can also produce pseudohypokalaemia)
- Hereditaryand acquired red cell disorders
Go to source: Spurious hyperkalaemia — Smellie 334 (7595): 693 — BMJ
Spurious results relating to temperature or storage can be moreproblematic. The response of whole blood to temperature varies.A fall in the serum potassium concentration is seen when samplesare stored at temperatures that are warm (25-30°C) but not sufficiently hot to cause sample deterioration (as a resultof stimulation of the red cell membrane ATPase, which regulatesexchange of potassium for sodium ions between the potassiumrich intracellular environment and the relatively low potassiumconcentration in serum). Average laboratory results for serumand plasma potassium in samples obtained from primary care havebeen reported to fall by up to 0.5 mmol/l in summer’s high ambienttemperatures.2 This effect may be greater with serum.3 Highertemperatures or long storage (overnight, for example) may lead to deterioration of the sample and large rises in potassium,although potassium stored at an ambient temperature of 18°Cfor up to 16 hours has been reported to be stable.4 Cold temperaturesdisable the membrane ATPase, leading to higher results,5 inwinter months and when samples are subject to long collectionruns to the laboratory. In primary care, samples cannot be takenclose to the point of analysis for rapid delivery without widespreadroutine use of point of care testing, which has its own difficulties.Laboratories could optimise carrying conditions and educate users: more systematic use of insulated specimen boxes in practices and temperature controlled transport systems in collection vansmay help.
Hyperkalemia Four pearls to keep in mind: * ECG changes may be subtle or even absent in the setting of significant hyperkalemia. In a retrospective review, ECG changes were seen in 43% of patients with potassium values ranging from 6.0 – 6.8 mEq/L and in only 55% of patients with values > 6.8 mEq/L (1,2). Many case reports in the literature describe patients with severe hyperkalemia who present with a normal ECG (1). * Calcium infusion for significant hyperkalemia has a rapid onset of action (3-5 minutes) and lasts for upwards of 1 hour. Because of the unpredictable nature of cardiac arrhythmias, authorities recommend that calcium infusion should be administered if any ECG change suggests hyperkalemia (1). If ECG changes are present, administration of IV calcium should normalize the ECG patterns. If it does not, a second dose can be administered (1). * Insulin administration decreases serum potassium levels within 15 minutes, with the effect peaking at approximately 60 minutes and lasting for 4 – 6 hours. The magnitude of the decrease is 0.5 – 1.0 mEq/L. In the presence of hyperglycemia (blood glucose >360 mg/dL), insulin alone should be given, as additional glucose leads to hypertonicity that can aggravate hyperkalemia (1). In children, glucose administration alone is often used to increase endogenous insulin secretion (1,3). * The use of IV calcium with concurrent digitalis toxicity is of concern because of the potential to exacerbate bradyarrhythmia and potentially cause arrest. Some authors recommend slow infusion of calcium if ECG changes due to hyperkalemia, such as loss of P waves or QRS complex widening, are present. In this situation, calcium should be diluted in 250 mL of D5W and given over 30 minutes (4). Alternatively, cases have been reported in which cardiac arrhythmia improved only after administration of digoxin Immune Fab. References: (1) Sood MM, et al. Emergency Management and Commonly Encountered Outpatient Scenarios in Patients With Hyperkalemia Mayo Clin Proc 2007;82:1553-1561. (2) Acker CG, et al. Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines. Arch Intern Med. 1998;158(8):917-924. (3) Advanced Life Support GroupPaediatric Life Support: The Practical Approach. 2nd ed. London, England: BMJ Publishing Group; 1997:254. (4) Parham WA, et al. Hyperkalemia revisited. Tex Heart Inst J. 2006;33(1):40-47.
Bicarb For Hyperkalemia: Not What You Were Taught (from EMEDhome)
The purported effects of a bolus injection of sodium bicarbonate in the emergency treatment of hyperkalemia pervaded the literature until the past decade. Emergency physicians are often taught that IV sodium bicarbonate is part of the treatment “cocktail” for hyperkalemia. This dogma was based upon studies using a prolonged (4-6 hours) infusion of bicarbonate (1,2). It has now been clearly demonstrated that short-term bicarbonate infusion does not reduce plasma potassium concentration in patient with dialysis-dependent renal failure, implying that it does not cause potassium shift into cells (1).
Whether bicarbonate infusion might enhance insulin-mediated cellular potassium uptake remains unresolved by two contradictory studies (3,4). This is not meant to imply that sodium bicarbonate should be withheld from the hyperkalemic patient with metabolic acidosis; rather, no short-term effect on the potassium concentration should be anticipated.
References: (1) Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251. (2) Fraley DS, Adler S. Correction of hyperkalemia by bicarbonate despite constant blood pH. Kidney Int 1977;12:354-60. (3) Allon M, Shanklin N. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol Am J Kidney Dis 1996;28:508-14. (4) Kim HJ. Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients. Nephron 1996;72:476-82.
There are a variety of drugs which can result in hyperkalemia, via a variety of mechanisms. Here are a list of some of the common offenders, categorized loosely based on mechanism, though admittedly there is some overlap between categories:1. Drugs which cause translocation of K from the intracellular to the extracellular fluid: these include succinylcholine, isoflurane, minoxidil, and beta-blockers.2. Potassium-Sparing Diuretics: drugs such as spironolactone (mineralocorticoid receptor antagonists) and amiloridine/triamterene (blockers of the ENaC) are common causers of hyperkalemia.3. Inhibitors of renin-angiotensin-aldosterone axis: ACE-inhibitors, angiotensin receptor blockers.4. Hyperosmolarity: hyperosmolarity induces water efflux out of cells, and by solvent drag increases intravascular potassium concentrations. Drugs such as mannitol can therefore cause translocational hyperkalemia.5. NSAIDs: NSAIDs can lower renin secretion, which is normally mediated in part by locally-produced prostaglandins.6. Bactrim: the hyperkalemia induced by Bactrim is via an ENaC inhibitory effect exerted by the trimethoprim moiety. Pentamidine induced hyperkalemia via a similar mechanism.7. calcineurin inhibitors (e.g., cyclosporine, tacrolimus): it is postulated that these medications inhibit renal tubular responsiveness to aldosterone.8. heparin & ketoconazole: these drugs may be associated by hyperkalemia by inhibiting aldosterone synthesis.9. digitalis: digitalis inhibits the Na-K ATPase (which pumps 3 Na out of the cell and 2 K in); as such, it can result in hyperkalemia and a variety of cardiac arrhythmias.
If wide QRS:1 amp CaCl by slow push or if poor IV line, 2 amps CaGluc by slow infusion10 units insulin &2 amps D50 (50 G)Albuterol 5 mg nebulizedNaBicarb 150 meq in IV fluids, administer at a rate commensurate with volume status250 ml Normal SalineKayexalate 60 GIf volume overloaded, Lasix 40 mg ACEARBsNsaidsCOX2Potassium Sparing Diuretics
Potassium Pathophysiology (From Life in the Fast Lane Blog)
- Serum potassium is normally maintained between 3.5 -5.0 mmol/L
- Hyperkalaemia is defined as a potassium level greater than 5.5 mmol/L
- Hyperkalaemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors.
Classic Causes of Hyperkalaemia
- Excessive exogenous potassium load (Increased Intake)
- Potassium supplements (IV or Oral)
- Excess in diet
- Salt substitutes (e.g. potassium salts of penicillin)
- Excessive endogenous potassium load (Increased Production)
- Extensive burns
- Tumor Lysis Syndrome
- Intense physical activity
- Trauma (especially crush injuries and ischaemia)
- Redistribution (Shift from intracellular to extracellular fluid)
- Acidosis (metabolic or respiratory)
- Insulin deficiency
- Digoxin (acute intoxication or overdose)
- Hyperkalemic familial periodic paralysis
- Diminished potassium excretion(Decreased Excretion)
- Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
- Decreased mineral corticoid activity
- Defect in tubular secretion (eg, renal tubular acidosis II and IV)
- Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics, ACE Inhibitors)
- Pseudohyperkalemia (Factitious)
- Haemolysis (in laboratory tube) most common
- Venepuncture technique (e.g. prolonged tourniquet application)
From Renal Fellow Network:
Hyperkalemia can be a life-threatening condition. Nonetheless, in transplant recipients with delayed graft function, there is a tendency to try to avoid dialysis early after transplant. The reason behind this approach is that a session of hemodialysis further delays the recovery from ATN/ischemia and significantly drops urine output afterwards (indirect evidence – no randomized trials available). This is potentially related to hemodynamic changes associated with the dialytic procedure, even in the absence of volume removal (osmotic shift). So what are your options if you have a patient with a potassium of 6 about 72 hours after transplantation with low urine output?
First option, if he doesnt have ECG changes, is to try a loop diuretic at a high dose to see if he can respond to that and produce some kaliuresis. If he doesnt respond and has had a bowel movement since surgery, I would do a trial of sodium polystyrene sulfonate binding resins (e.g.Kayexalate). Now, it gets into a little controversial territory.
Last year, Sterns et al. in an editorial on JASN concluded that the use of SPS resins is largely unproven and potentially harmful, and should be considered only as a last resource. That was quite shocking to me since I have used it many times and I always saw a decrease of serum potassium levels. I do acknowledge the increased risk of colonic necrosis that has been reported with sorbitol commonly added to Kayexalate to increased bowel movements, but I was prescribing only mixed with water and other than the low palatability of the solution, no major side effects were seen.
Actually, after reviewing the literature, the most common side effects reported are nausea, vomiting and constipation. I was able to download the first trial using SPS resins published in the NEJM in 1961! Small number of patients (n=22) but the results looked quite impressive, since a median dose of 40g was able to decrease the potassium level by 1mEq/L and additional doses led to further decrease in levels (median decrease of 1.8mEq/L). It is important to know that the peak effect of SPS takes about 4-6 hours, so if ECG changes are present, you will need to use IV calcium for membrane protection and albuterol/insulin+dextrose for transient K+ shift to the intracellular. The majority of reported complications were associated with SPS/70% sorbitol enema. This combination should be avoided, especially in patients with compromised GI function (e.g. ileus post-op). As an alternative, lactulose could be used to stimulate the GI tract. Finally, Kayexalate releases sodium ions after uptake of potassium, so there is a potential side effect of edema due to sodium retention (not significant in 1-2 doses).
Is there a way to estimate how much resin you will require? Efficiency of a resin is dependent on several factors, including intrinsic properties of the resin (capacity and ion selectivity), [K+] and [Na+] extracellular concentrations and colonic transit time. In general, a decrease in 0.5mEq/l [K+} would require at least 30g of Kayexalate.
Going back to our patient: After a diuretic trial, I would recommend two doses of 30g of Kayexalate mixed with water PO with repeat labs in 8-12 hours. Caveat, if the patient has no urine output or have other potential indications for dialysis (e.g.volume), you should just buy the bullet and dialyse him.
More acute hyperkalemia management on this blog. Picture above from Jackson Hole – insane ski destination…Bicarb Stuff From Graham:Quick summary: We’re all taught bicarb works within 30 minutes, byintracellular shift/exchange of potassium ions for hydrogen ions, yadayada yada. That really doesn’t appear to be the case. I think in theED we’re sometimes taught to just give them an amp or two of sodiumbicarb, but that appears to have NEVER been studied.All the studies have really looked at bicarb infusions over hours, andif there’s any change to be found, it’s maaaybe at the 6 hour mark(after 6 hours of bicarb infusion, in patients who are already gettingdialysis). Other studies with bicarb infusions show no statisticallysignificant change, either. (One study that took patients and put themon a high or low dose bicarb infusion for an hour actually found ahigher potassium levels after the infusion.) Probably the best study(Blumberg, 1992) found only a 0.5-0.7 drop, but they then attribute half the drop to the expansion of the ECF due to all the sodium the patients got.Insulin definitely works. Albuterol works (but the studies are smalland they usually give a good 10-20mg of it nebulized). There have beena few studies looking at combining bicarb + either of these othermethods, and it looks like the bicarb *probably* DOES have somesynergistic effect (it lowers the potassium more than just, say, albuterol alone). But by itself? Bicarb is probably pretty worthless.Reviewing the literature, it seems like the insulin/D50, albuterol (? Lasix, not much literature on it) methods are the way to go. I know before I read this literature I felt better because I’d given theperson kayexalate, or I’d given them bicarb, but really, the othermethods are much more likely to keep the patient alive on the floorfor 6 hours while they await their dialysis, without putting them intoflorid fluid overload.I’ve summarized the literature and we can send you the articles ifyou’re curious (but they’re old, so the PDFs are big and it’s about9MB). Pretty interesting stuff.Sincerely,Graham WalkerKim MedlejBurnell, 1956Looks like this is where a lot of it started. Many articles from the70s/80s cite this one. There’s very little on their methodology, butthey have some pretty cool graphs that show an inverse relationshipbetween pH and serum potassium concentration.Schwarz, 1959Case series of hyperK patients who had EKG changes who got better withbicarb. (Some of them got calcium as well, others required “5-10 gramsof bicarb a day,” others got bicarb + blood transfusion.)Fraley, 1977Methods: Took 14 hyperK patients, gave them bicarb infusions over 4-6hours. Checked K every hour. Results: Divided groups retrospectively into “constant pH” and”changed pH” groups. Both groups showed decreases in their potassium, ~1.6-1.8mmol/L (never seen this significant of a drop reproduced). Blumberg, 1998Methods: Took 10 HD patients, checked their K (along with other labs),gave them a bunch of different agents for changing K (bicarb, insulin,epi drip, regular dialysate), and then checked their labs after anhour. For bicarb, it was 8.4% in water, 4mmol/min, for 1 hour only. They also tried a isotonic bicarb infusion of 1.4%.Results: The K actually went UP after both bicarb infusions.They conclude that bicarb didn’t work, but in the past it’s workedover longer periods of time. So then they do …Blumberg, 1992Methods: Took 12 hyperK (>5.8) patients on dialysis, gave a bicarb(8.4% in free water) infusion 4mmol/min x1 hour, then 1.4% bicarb inwater infusion 0.5mmol/min hours 2-6 and checked potassium levelsthroughout the time on dialysis. Also checked an EKG.Results: Average K was 6.0. K dropped at 4-6 hours, by 0.5-0.7, andthey believe that half of the drop is probably due to the huge sodiumload and increase in the extracellular fluid compartment.Allon, 1996Methods: Took 8 HD non-HyperK patients, put them through differentcombinations to lower their K (bicarb infusion, saline infusion,bicarb+insulin, saline+insulin, bicarb+albuterol, saline+albuterol).Results: Bicarb or saline infusions didn’t work. Anything with insulinor albuterol the combination worked, lowered them from 0.5-0.8,depending on the group. Of note, bicacrb + albuterol worked betterthan saline + albuterol (see Kim, 1997).Kim, 1997 Methods: Took 9 HD hyperK patients, gave them separate or combinedbicarb infusions (1/2 hour long) along with nebulized albuterol,checked K before and after. Thought maybe there would becombined/synergistic effects of the two meds.Results: Bicarb alone didn’t change the potassium. Salbutamol alonedropped the K by 0.6, and salbutamol + bicarb dropped the K by 0.9.Kaplan, 1997Methods: Took 8 dogs, gave potassium infusion until they gotconduction disturbances, then backed down on the K, and gave eitherbicarb infusion (1.05% over 1 hour), bicarb bolus (8.4% over 5minutes, then saline), or “saline” therapy (hypertonic saline 8.4%bolus + normal saline). Measured K before and after.Results: Saline worked just as well as bolus. Infusion worked betterthan both (but not statistically significant). Change was 1-2mmol/L.Review Articles:Kim, 2002: Don’t recommend bicarb, especially as a single agent,especially in dialysis patients. “Should not be used.”Weisberg, 2008: Definitely doesn’t work short-term, but might still beuseful for temporizing hyperK. “It has now been clearly demonstratedthat short-term bicarbonate infusion does not reduce PK in patientswith dialysis-dependent kidney failure, implying that it does notcause K shift into cells. Infusion of a hypertonic or an isotonic bicarbonate solution for 60 mins has been shown to have no effect onPK in dialysis patients, despite a substantial increase in serumbicarbonate concentration.” “Sodium bicarbonate should not be withheldfrom the hyperkalemic patient with met- abolic acidosis; rather, thatno short-term effect on the PK should be anticipated.”Rachoin, 2010: “When treating hyperkalemic patients, hospitalistsshould use sodium bicarbonate to potentiate urinary elimination ofpotassium and should consider administering it either withacetazolamide or a loop diuretic, anticipating a lowering effect aftera few hours.26 It should be avoided in patients with volume overloadand anuria. Immediate translocation of potassium into cells is bestachieved by insulin and b-2 agonists.”
Martin et al. Ionization and hemodynamic effects of calcium chloride and calcium gluconate in the absence of hepatic function. Anesthesiology. 1990;73:62-65
Cote et al. Calcium chliride versus calcium gluconate: comparison of ionization and cardiovascular effects in children and dogs. Anesthesiology 1987;66:465-70
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