Hyper Kale Mia Edited

8/8/2019 Hyper Kale Mia Edited

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Hyperkalaemia

Adapted from source

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P resentation Objectives

Discuss the emergent management of acutehyperkalemia in unstable adults.

1) Discuss and understand the various tests for

hyperkalemia.2) Discuss and understand the physiology behind the

various treatments for hyperkalemia.3) Discuss the evidence for, and strength of, the various

different treatment possibilities for hyperkalemia.

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N ot P resentation ObjectivesThis talk is not designed to focus on:

management of chronic or acute-on-chronichyperkalemia (in patients with ESRD, patients who are

on dialysis, et cetera). etiologies of hyperkalemia clinical findings in hyperkalemia extra-cardiac complications of hyperkalemia disposition of hyperkalemic patients

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G rab chart and head into patient s cubicle.

First impressionMr. S. is lying in a bed.He is a big old man (~112kg, 67yrs).He is moving and looking around.He is very diaphoretic.He looks like hell.

What do you want to do now?ABC s and vitals!

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ABC sP t is speaking, but responding inappropriatelyto my questionsVital signs

Afebrile, HR 67, RR 24, B P 103/67, 100% on 6L byNP , BSL 6.8

Are you going to call a code, or are you going to

keep going for now?Keep going for now.

Think about calling a friend.

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The EKG and AB G are being done Time for 60seconds of history.

P t is BIBA, known case of DM & HT N .P ast history of IHD and AF.On digoxin, Beta Blocker and on 101 moremedications.Has been non-acute for well over 11 months.Self-ambulating

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N ormal lung, heart, G I, kidney

N o P SurghxN o allergiesN on-smoker, light drinker, no drugs

Only close relative is a brother in SydneyN o FHx

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U nremarkable events at home N

o falls or accidents N o worrying fluctuations in his behaviour or his

LOC G radual history to a state of mild-moderate

confusion.G ets routine follow up once a month withhis GP .

Last B/W was three weeks ago:N ormal CBC/diff N ormal lytesN ormal B UN /Cr

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EKG is up


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Junior Doctor s refresher

What are 6 EK G signs of hyperkalemia (in order of increasing severity)?

P eaked T s Shortened QT Lengthened P R QRS widening Flattened P s

Sine-wave ( VF/asystole)

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Blood gas is upLess interestingly:

7.42/32/22/100% (on 6L)More interestingly:

N a: 137K: 8.6

HCO3: 20Cl: 102

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So it s the real thing?

Well let s see. P t clinically unwell Appropriate EK G manifestations Level confirmed by AB G This talk is on the treatment of acute

hyperkalemia in unstable adults.

So, ehh yeah. It s the real thing.

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Why ask if it s real?Because the #1 cause of hyperkalemia is

pseudohyperkalemia , secondary to:in vitro hemolysis small needle high-vacuum vacuum tube tourniquet use

Labs techs will usually recognize the tell-tale pinkserum that accompanies hemolysis, and will reportthis.

extreme leukocytosis K released from WBC s

severe thrombocytosis K released from platelets

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How should I treat this patient?

Call the medical P HO or ED SMO and let them dealwith it.

Yes this is one option But lets put on the big-boy pants for a little while here

and pretend that we are the ones who have to save thispatient.

(That being said, getting someone to phone yourmedical P HO or SMO while you are saving thepatient is probably not the worst idea in theworld.)

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So, how should I treat this patient?

Five general avenues of treatment(you d better get at least four) :

1) Stabilize the heart2) Stop giving K3) Shift K intracellularly

4) G et the K out of the body5) Fix the underlying cause

We will discuss the first four avenues.19


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#1- Stab ilize th e h e art


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The cardiac sx of hyperkalemia are related toimpaired neuromuscular transmission.

The resting membrane potential (rmp) is usually 70mV and (according to the N ernst equation) isgoverned (in part) by the ratio of intracellular

K/extracellular K.As this ratio drops, the rmp becomes less negative,and depolarization is increased at least, initially .

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But persistent depolarization leads to inactivationof the N a channels (which are the main mechanism

of neuron depolarization.)As such, an overall decrease in membraneexcitability is manifestedThis results clinically in:

muscle weakness decreased reflexes impaired cardiac conduction (i.e. bradycardias, widened

QRS, etc.)

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So how should I stabilize the heart?

N o secrets here 1 amp (10mL) of 10% Calcium gluconate slow IV push contains ~90mg elemental Ca Ca has no effect on the overall K level, but it does

antagonize the effect of increased extracellular K at thecardiac membrane ( by an unknown mechanism ).

As a result, the rmp drops back down to normal, theN a channels are reactivated, and cardiac conduction isrestored.

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When should I give the Ca?If possi b le, wait until after the EK G . the EKG offers a secondary method of confirming

the high K the EKG also offers a gross baseline estimate of

cardiac dysfunctionhelps one to determine the necessary aggressiveness of treatment

helps one to monitor the response to treatment

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That being said

In a patient with a high laboratory K whoappears grossly symptomatic and/orunstableDO N OT WAIT FOR THE EKG !G IVE THAT CALCIU M!

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The protective effect of Ca begins in 1-3 mins,but is relatively short-lived (20-40 mins).

As such, keep an eye on your EK G monitor whileyou initiate and continue other treatments.

Additional doses of Ca gluconate should be givenin 5-10 mins (and then q 15-30 mins) if malignantEKG changes persist on the monitor.

The risk of symptomatic hyperCa is small, butconsider re-checking an AB G with lytes if giving>3 doses.

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Danger danger.One possible etiology of hyperkalemia is digitalistoxicity.

Digitalis work by binding to (and inhibiting) the N a/Kpump on cardiac cell membranes.

As intracellular N a increases, a N a/Ca exchangerattempts to compensate by extruding N a inexchange for Ca.

The resulting increased sarcoplasmic Ca is thoughtto be responsible for digitalis increased inotropy.

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T he original Na/K exchanger b lockade , however, canlead to symptomatic hyperkalemia in digitalistoxicity

But realize that the hyperkalemia here is an effect notthe cause of the underlying problem

As such, giving Ca to fix the hyper-kalemia will only

allow even more Ca to enter the cardiac cell (via theN a/Ca exchanger)

This will worsen the effects of the underlyingdigitalis toxicity

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So don t give Ca if the patient is takingDigoxin?

It s not that simple A hyperkalemic patient taking Dig may not be

hyperkalemic from the Dig.You can t wait for a Dig levelDig levels don t necessarily correspond to dig toxicity in eitheracute or chronic overdosesVery few clinical findings will distinguish Dig-based from non-Dig-based hyperkalemia

yellow-green halos

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And finally

Even if the patient is hyperkalemic from his Digoxintoxicity, it is not as though the digitalis toxicity offersa protective effect against the hyperkalemia

i.e. the patient can still die from his hyperkalemia, just ashe could die from his digitalis toxicity

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So when should I give Ca to a patienttaking Dig?

Strong evidence-based guidelines do not exist: Kumar & Clark, 3 rd Edition

avoid Ca

U pToDate only given Ca when absolutely necessary

loss of P -waves QRS-widening

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#2 - Stop giving K

Reduce direct sources of potassium Replacement K in the IV K in NG tube feeds K in dialysate P otassium supplements (eg. Slow K) foods rich in potassium (bananas, oranges, leafy-green

vegetables) Transfusions of aged-blood Medications rich in potassium:

penicillincarbenicillin

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Also consider indirect increasers of K: K-sparing diuretics

several different mechanisms Beta-blockers

decrease renin release via direct B2-receptor action in thekidney

Therefore, non-selective B-blockers are much more likely tocause hyperkalemia than B1-selective blockers ACE-i

decrease the G FR (via effects on AII and the efferent renalvasculature)

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N SAIDSdecrease the G FR (via effects on prostaglandins andthe afferent renal vasculature)

Succinylcholinecauses transient K efflux secondary to muscle-cellmembrane depolarization.

High-dose TM P -SMXmay be an agent of hyperkalemia in patients withrenal insufficiency

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#3 Shift K intracellularlyThree main methods available:1) Insulin +/- glucose2) Sodium bicarbonate

3) Adrenergic-agonistsBear in mind

these are typically temporizing measures they are designed to buy you time while you reduce the body s

total potassium load

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Insulin +/- G lucose

N ote that it is the insulin not the glucosewhich lowers the K.

The glucose is merely used to increase the body s owninsulin secretion.

Insulin drives K intracellularly P roposed mechanism:

enhanced N a/K-pump activity in skeletal muscle

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How should insulin be dosed?

Several dosing regimens available: N o one method has been proven to be superior as

such always consider your individual patient.1) 10 U regular insulin + 1 amp of D50 (i.e. 50g of 50%

dextrose); IV push(Fast acting insulin is not required you are

not attempting to lower sugars.)

2) 1 amp D50 alone; IV push

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the insulin+glucose regimen may be more effective

than glucose alone in reducing potassium. the glucose-alone regimen does not carry the risk of

hypoglycemia present with the insulin+glucoseregimen.

both treatments will generally cause a drop in K of 0.5to 1.5 meq/L

this effect will usually take 15-30mins to begin, willpeak at ~1hr, and will last for 4-6hrs.

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Caution

A 10U dose of regular insulin will induce a significantdrop in glucose in most patients unless adequateglucose is also given up front

i.e. if given with an amp of D25 (as opposed to an amp of

D50), 10U

of regular insulin will cause sugars to fall below3mmol/L in up to 75% of initially normoglycemic patients

Therefore, monitor BSL closely when treatinghyperkalemia pts with insulin:

eg. 30mins, 60mins, 120mins

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Quick word on diabetics

Insulin is still effective at activating the N a/Kpump in diabetics (i.e. in reducing K) even inpatients who are resistant to insulin s glycemic

effects.Regimens:

if patient is hyperglycemic, give insulin alone. if patient is normoglycemic, give insulin+glucose.

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Sodium BicarbonateP roposed mechanism:

Raising the serum pH with N aHCO3 results in therelease of H + from cells (buffering action).

This increase in H+

, (in order to maintainelectroneutrality) drives K + intracellularly In addition , HCO3 also appears to directly reduce

serum K + by an unknown but pH-independent

method.

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P rovisos

As monotherapy, N aHCO3 tends to be: more effective in:

pts with a metabolic acidosis accompanying the hyperkalemia

(does this make sense?) less effective in:

pts with advanced renal failure

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N aHCO3 Dosing

N o strong evidence exists as to the optimal dosingamount or strategy:

As such, the following strategy is suggested as one that isboth simple and fast.

1-2 amps (50-100meq) of N aHCO3; given one afteranother, both via a slow IV pusha 3 rd amp may be given in 30 mins if pt remainsdangerously hyperkalemic

Bicarb will begin to work in 5-10mins, and willcontinue to work for 1-2hrs

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Beta-agonistsMechanism

The B-agonists work in the same manner as insulinby increasing N a/K pump activity

B-agonists that can be used include: Ventolin

can be given via N eb or intravenously Epinephrine

can be given via a slow IV infusion(less commonly used than Ventolin for both logistical andmedical reasons.)

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DosingVentolin

N ebulizer: 10-20mg (large dose) given over 10mins begins to work in 15-30mins, peak effect in 90mins ,

lasts 3-4hrs IV:

0.5mg IV given over 10mins begins to work in minutes, peak effect in 30mins

Both regimens will cause a drop in plasma K of 0.5-1.5meq/L, but IV ventolin works faster The nebulized route, however, might be easier to initiate in a

hurry.

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CaveatsB-agonist use is obviously less advisable inpatients with heart disease.

most typical side effect would be a mild tachycardia

that being said, one could potentially induce angina inpatients with coronary disease especially if using Epinephrine

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#4 G et K out of the bodyOnce again, three main methods:

1) Cation-exchange resins2) Diuretics

3) Hemodialysis

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Cation-Exchange ResinsThe most commonly used cation-exchange resin isKayexalate (sodium polystyrene sulfonate).Kayexalate draws potassium into the G I tract (in

exchange for sodium) via N a/K pump in the gutlumen.

Its primary site of action is in the large intestine

Once drawn into the gut, K is bound to the resinand excreted in the feces.

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Each gram of resin binds ~ 1meq of K in exchangefor ~2-3 meq of N a.

In patients with CHF, this large sodium load can lead toproblems with symptomatic fluid overload.

In the process of removing K from the body,

significant amounts of Ca and Mg also tend to beremoved.

As such, it requires an astute physician to closelymonitor these secondary (as well as the primary)

electrolytes following cation-exchange-resinadministration.

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DosageOral dosing

25g of Kayexalate P O or NG begins to work in ~2hours , can be repeated every 4-

6hrs as necessaryRectal dosing

50g of Kayexalate as a retention enema must be retained for at least 30mins, and preferably for

up to 6 hours!! Begins to work in ~30mins , and can be repeated every

2-4hrs as necessaryEither method can reduce serum K by 0.5-1meq/L.

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Drawbacks

As mentioned, resins can cause: hypernatremia ( fluid overload) hypocalcemia hypomagnesemia

The resins also tend to be dramatically constipating,and should be given with a laxative such as sorbitolor lactulose

Actual Kayexalate -brand cation-binding resin is alreadymixed in sorbitol and requires no further laxative to beadded.

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The most serious possible adverse effect of cation-exchange resin administration is the possibility of bowel necrosis.

this risk is typically very small (


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Diuretics

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K+ absorption in the kidney takes place in theP

CT and the loop of Henle. Therefore, by the end of the loop of Henle, all K

resorption that is going to take place, has takenplace.

In acute hyperkalemia, two types of diureticsare commonly used to induce a K-wasting:

Thiazide-type diuretics Loop diuretics

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Thiazide-type diuretics

Thiazides act at the loop of Henle and at theDCT, by blocking the Cl portion of the N a/Cl

symport.This prevents N a and Cl from entering thetubule, which in turn induces a N a and Cldiuresis.

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Thiazides cause K + loss by two main

mechanisms:1)The induced N a loss will stimulate aldosterone

production (in an attempt to conserve N a in theDCT and the collecting tu bules ).

-As such, N a will be retained inexchange for K in these areas.

2)Loss of Cl will result a hypochloremic alkalosis.-The kidney will attempt to

compensate by retaining H+

and Cl-

in exchange for potassium.

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Loop diureticsLoop diuretics act similarly to thiazidediuretics, but are specific for the N a/K/Clsymport in the loop of Henle (not just theN a/Cl symport).

These also act by binding to the Cl site, andblock tubule resorption of all three ions ( N a, K,& Cl).Loop diuretics therefore produce a more

profound K-loss than thiazides. Directly block K resorption in addition to inducing

the subsequent K losses that result as the bodyattempts to conserve N a and Cl (as previouslydiscussed).

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Since loop diuretics act faster and producea more profound K loss than thiazide-typediuretics, they tend to be the diuretics of choice in acute hyperkalemic crises.

Lasix 40-80mg IV push

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Do s ag e

H di l i


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HemodialysisHemodialysis corrects hyperkalemia rapidly and effectively.

starts to work in minutes and can remove 25-50 meqof K per hour removes K from the body many times faster than

peritoneal dialysis

May represent the only feasible option for hyperkalemia Rx inseveral settings: when conservative Rx has failed, or is not working rapidly

enough in pt s with ESRD (in whom many of the conservative Rx s are

less effective) when the hyperkalemia is the result of severe

rhabdomyolysis

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Emergent dialysis for acute hyper-kalemia willobviously have to be arranged in consultationwith N ephrology +/- the IC U .

They may choose to lower the K with a dialysatebath ranging anywhere from 0 to 4 meq/L

lower-K baths will remove K more rapidly butincrease the chance of cardiac dysrhythmias andaccidental hypokalemia.

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That s pretty much it.

So one example of a typical treatmentregimen for severe acute hyperK might be:

Ca gluconate (if no contraindications)Stopping all extraneous K sourcesInsulin+glucoseN aHCO3Ventolin nebs

Kayexalate retention enemaIV LasixN ephro/IC U consult for possible dialysis

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Hyper Kale Mia Edited