An unstable wide complex tachycardia resistant to electrical cardioversion


Thanks to our electrophysiologist, Rehan Karim, for his help with this post.

Case

A very elderly inpatient suddenly had a rapid pulse by oximetry.  The nurse put him on the monitor and noticed a wide complex tachycardia.  The patient was alert with a normal blood pressure.  He had a history of myocardial infarction, with a known lateral wall motion abnormality and a chronic total occlusion of the circumflex.

A 12-lead ECG was recorded.
Click on image to enlarge
Regular, Monomorphic, Wide complex Tachycardia (WCT) at a rate of 190.
What do you think?



















Interpretation: This is clearly Sustained Monomorphic Ventricular Tachycardia.

You may say that interpretation does not matter because electrical cardioversion works for any regular WCT, but you'll see in this case that electricity did NOT work and that interpretation may indeed matter.

How do we know it is VT?
Pretest probability
    1) Most regular WCT is VT
    2) In elderly patients, an even higher percentage is VT
    3) Patients with a history of MI have scar tissue and have an even higher risk of VT
    4) When there is poor LV function, VT is more likely still

Post-Test probability (the ECG alone, regardless of clinical factors)
    1) The QRS duration is very long (wide).  In lead V3, it appears to be about 180 ms. (1)
    2) There is a monophasic R-wave in lead V1 (RBBB morphology but without the typical rSR' of true RBBB).(2)
    3) The initial part of the QRS is very wide.  aVR takes 80 ms to reach its peak.  Moreover, the impulse initiates towards aVR, turns around and goes away (toward lead II), then turns back to aVR [see (4) below].(3)  
    

(1)  In WCT, a QRS duration of greater than 140 ms favors VT with only moderate specificity.  Duration of 160-180 ms strongly favors VT.
(2)  A monophasic R-wave in V1 heavily favors VT.
(3)  In VT, the impulse is initiated in myocardium, not in conducting fibers, and thus travels slowly before it arrives at a conducting fiber.  Therefore, the initial part of the QRS is slow (wide).  In SVT with aberrancy, the impulse is conducting through Purkinje fibers and thus the initial impulse is relatively narrow.
----For cases in which there is an LBBB-type morphology in lead V1 (small r-wave followed by deep S-wave): if there is any precordial lead which has an onset of R-wave to nadir of S-wave of greater than 100 ms, then VT is very likely.  Even though in V2 this interval is 120 ms, the rule does not strictly apply here because there is RBBB (not LBBB) morphology in lead V1 (an upright R-wave).
(4) Axis (not as helpful here as one might expect): As a general rule, with exceptions: in VT, the impulse starts in the ventricle (inferior and leftward) and travels up and to the right, resulting in an upright R in aVR.  This results in a "Northwest" axis, at between -90 and -180 degrees.  
----In this case, although aVR appears all upright, the axis is more complex.  Note that leads II, III, and aVF are positive, indicating an inferior axis.  Why the discrepancy?  If you look very closely, you'll see that the impulse starts toward aVR, turns back toward the inferior leads, and then turns toward aVR again, all in very rapid succession.  Such a convoluted pathway is also a good sign of VT.

There was a suggestion that retrograde P-waves were present and that this might indicated SVT.  However, I don't see any here, AND the presence of retrograde P-waves does not help to differentiate VT from SVT.   Retrograde P-waves can be seen both in SVT and VT.
----AV dissociation (P-waves, not retrograde, out of sync with the ventricle) heavily favors VT

See this post for an more complete overview of the ECG diagnosis of wide complex tachycardia:
http://hqmeded-ecg.blogspot.com/2017/01/wide-complex-tachycardia-and-cyanosis.html

Clinical Course

--The blood pressure began to drop.
--Adenosine 6 mg, then 12 mg was given without any change.
--Amiodarone 150 mg was given without change.
--A bedside ultrasound showed poor LV function.
--The patient was given midazolam to prepare for electrical cardioversion
--The BP dropped to 50-60 systolic after midazolam.
--He was shocked multiple times with biphasic synchronized cardioversion at 200 J.  The rhythm reportedly converted, then reverted to VT each time.
       --The patient was greatly distressed by the shocks, in spite of midazolam.
--The patient was intubated and given another 12 mg of adenosine without change.
--Another 150 mg bolus of amiodarone was given.
--Mg 4 g IV was given
--Ultimately, lidocaine 100 mg bolus x 2 was given
--Patient converted to a bradycardic rhythm:

Potassium was 4.1 mEq/L

Slow junctional rhythm.
Notice very tall R-waves in V2-V4, consistent with old posterior MI
ST depression in V2-V4 is consistent with acute ischemia or old MI

A previous ECG showed similar R-waves, consistent with the old "lateral" MI and chronic total occlusion of the circumflex.


Transcutaneous pacing was successfully initiated.

When pacemaker temporarily stopped, patient was in sinus rhythm on the monitor.

Shortly after, this ECG was recorded:
Sinus rhythm
Less ST depression
Same tall chronic R-waves



An echocardiogram was done:

Decreased left ventricular systolic performance moderate .
Regional wall motion abnormality-inferior .
Regional wall motion abnormality-inferolateral .
Regional wall motion abnormality-anterolateral .
The estimated left ventricular ejection fraction is 30-35 %.


Clinical Course
Later, recurrent VT was terminated again with lidocaine.

--Lidocaine is a parenteral type Ib antidysrhythmic.  Therefore, the patient was started on started on oral mexiletine, another type Ib antidysrhythmic.
--There was discussion of placing an implantable cardioverter-defibrillater.
--The VT was thought to be due to scar from old myocardial infarction.
--There was a plan to also keep K above 4.0 and Mg above 2.0.


Is this incessant VT?

While it certainly is incessant (it is not converting with multiple therapies), "incessant VT" is a term usually used for sustained VT that is not causing any hemodynamic compromise.  It is defined by at least 2 VT/VF episodes requiring intervention over a 24-hour period.  So this is not standard incessant VT, as this patient was not stable.

Treatment of Unstable Sustained Monomorphic VT (SMVT)

For initial conversion:

--Adenosine will not work for this VT
    (Adenosine does work for some VT associated with structurally normal hearts, especially right ventricular outflow tract VT -- see this case.  These cases generally are in healthy people, are not usually unstable, and are not very wide).

---If you think it is SVT with aberrancy, adenosine is safe in VT and may be worth a try.  In this case, the probability of SVT was very low.

--Synchronized electrical cardioversion is indicated, using safe and effective sedatives.  If the patient is very unstable with altered mental status, cardioversion may be done without sedation.
          --Occasionally, the machine's algorithm cannot differentiate the QRS from the T-wave, and cannot synchronize, and therefore the shock does not fire at all.  In such a case, synchronization must be turned off.
         This patient received midazolam and the shocks greatly disturbed him and he feared there would be more.  Midazolam is also NOT safe.  It causes hypotension and respiratory depression.  Etomidate (causes annoying myoclonus) or ketamine (may result in emergence dysphoria) are safer.  However, any sedative can cause some hemodynamic compromise and respiratory depression, no matter its reputation.

If the VT does not convert, or converts and recurs, then medication will be needed:

--Always replete K to above 4.0 mEq/L and Mg to above 2.0 mEq/L.

--Amiodarone bolus and infusion can be very effective and is a good first line agent.  150 mg over 10 minutes followed by infusion of 1 mg/min.  The bolus can be repeated to a maximum total dose of 2.2 g over 24 hours.  There are potential adverse events, including hypotension.  In particular, the diluent can cause hypotension when amio is given too rapidly, and amio has some beta blocking effects.

--Lidocaine is less likely to be effective, but also with fewer adverse events. So it is well worth a try.  Loading must be given in several boluses, as it is an intracellular drug and takes a few minutes to redistribute from serum.  For a standard sized person, give an initial 100 mg over 2 minutes, then 50 mg q 5 minutes x 3 for a total of 4 boluses in 15 minutes.  If VT recurs, then an infusion of 1-4 mg/min.

--Beta blockers may work and are frequently used due to the high catacholamine state (which may be exacerbated by shocks with inadequate sedation).  However, of course, they are potentially hazardous in patients with poor LV function.  I have always been too nervous to give metoprolol to these patients; I have used esmolol.  Our electrophysiologist wrote this:
     "Beta blockers can be used in stable patients if other agents fail, and we don’t want people to take message that they should not use it at all. The key is beta blockade and blocking sympathetic activation is important in these situations of incessant VT where other therapies fail. Actually sometimes we deeply sedate patients to take away sympathetic stimulation and that by itself helps. In fact, some big centers in extreme cases do cervical sympathectomy as last ditch effort."  He added that he finds that esmolol often causes more hypotension than metoprolol. After administration of beta blockade, attempt DC Cardioversion again.

--Pace termination.  If these therapies fail, our electrophysiologist writes:  If the VT had not terminated after lidocaine, "I probably would have taken him to cath lab for temporary pacemaker and 'pace-termination' before considering procainamide (of course depending on hemodynamics at the moment)."

--Procainamide may work if the above do not, but is especially hazardous with decreased LV function and should be given very slowly, if at all.  Give 20 mg/min to a total of 15 mg/kg until the arrhythmia terminates, the BP drops, or the QRS is prolonged by more than 50%.  Procainamide slows the VT rate and though it often causes hypotension, it can sometimes be hemodynamically beneficial if the slower rate allows for more ventricular filling time.  Maintenance infusion if necessary.

--IV sotalol (100 mg IV over 5 minutes) was found to be more effective than lidocaine (100 mg IV over 5 minutes) when administered to patients with spontaneous hemodynamically stable sustained monomorphic VT in a double-blind randomized trial within a hospital setting.  However, if the QT is prolonged after you've already given a QT prolonging drug like amiodarone, it is relatively contraindicated.  And you can't measure the QT while the patient is still in VT!
Ho DS, Zecchin RP, Richards DA, Uther JB, Ross DL. Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet. 1994;344:18–23.





AHA guidelines:

[PDF] 2010 American Heart Association

guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science  (Full text)




Learning Points:

1. Learn to identify VT
2. Adenosine will not work for this VT.
3. Cardiovert unstable VT at 200 J biphasic
4. If no conversion, or if reversion, use amiodarone
5. If amio does not work, try lidocaine
6. Consider beta blockade.
7. Consider pacing termination
8. Only then consider procainamide, as it is particularly hazardous.









Stable VT

Here is a great review of the literature on stable VT at EM Docs:

STABLE MONOMORPHIC VENTRICULAR TACHYCARDIA MANAGEMENT IN THE ED

Quick summary: For stable VT, Procainamide may be a first choice for those with good LV function, but any of amiodarone, lidocaine, or sotalol may work.  Obviously, electricity is likely to work as well, and (just like with unstable VT) this is usually my first choice, saving medications for VT refractory to electricity, or recurrent.



Other literature

Incessant VT (stable persistent or recurrent VT) responds best to amiodarone, lidocaine may also work, but in this randomized crossover study, amiodarone performed better than lidocaine:
http://www.sciencedirect.com/science/article/pii/S0002914902027078

In this study of refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation, the event rate decreased with increasing doses of amiodarone: median values were 0.07, 0.04, and 0.02 events per hour for the 125-, 500-, and 1000-mg dose groups (mg per hour, with 150 mg boluses for breakthrough VT), respectively, representing a significant decrease from baseline event rates.  There was a 26% rate of hypotension as an adverse effect.
http://circ.ahajournals.org/content/92/11/3264.long


Cardiac Arrest

Amiodarone and lidocaine in cardiac arrest or to prevent recurrent arrest

Some randomized studies show higher rates of ROSC and hospital admission for out-of-hospital cardiac arrest treated with amiodarone:
http://www.nejm.org/doi/full/10.1056/NEJMoa013029#t=abstract (amio vs. lidocaine)
http://www.nejm.org/doi/full/10.1056/NEJM199909163411203#t=abstract (amio vs. placebo)

In this study, both were superior to placebo for witnessed arrest, but neither was superior to each other:  http://www.nejm.org/doi/full/10.1056/NEJMoa1514204#t=abstract

Preventing Recurrent Arrest after VF:
On the other hand, in this study, lidocaine was very effective in preventing recurrent ventricular fibrillation after ROSC: http://www.sciencedirect.com/science/article/pii/S0300957213003031.  Here is the abstract:

Resuscitation. 2013 Nov;84(11):1512-8. doi: 10.1016/j.resuscitation.2013.05.022. Epub 2013 Jun 3.
Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest.

Abstract
BACKGROUND:
Antiarrhythmic drugs like lidocaine are usually given to promote return of spontaneous circulation (ROSC) during ongoing out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation/tachycardia (VF/VT). Whether administering such drugs prophylactically for post-resuscitation care after ROSC prevents re-arrest and improves outcome is unstudied.
METHODS:
We evaluated a cohort of 1721 patients with witnessed VF/VT OHCA who did (1296) or did not receive prophylactic lidocaine (425) at first ROSC. Study endpoints included re-arrest, hospital admission and survival.
RESULTS:
Prophylacic lidocaine recipients and non-recipients were comparable, except for shorter time to first ROSC and higher systolic blood pressure at ROSC in those receiving lidocaine. After initial ROSC, arrest from VF/VT recurred in 16.7% and from non-shockable arrhythmias in 3.2% of prophylactic lidocaine recipients, 93.5% of whom were admitted to hospital and 62.4% discharged alive, as compared with 37.4%, 7.8%, 84.9% and 44.5%, of corresponding non-recipients (all p<0 .0001="" 0.34="" a="" adjusted="" admission="" analysis="" and="" arrest.="" arrhythmias="" associated="" association="" beneficial="" confidence="" covariates="" discharge="" for="" from="" higher="" hospital="" however="" improved="" in="" incidence="" independently="" interval="" lidocaine="" lower="" nonshockable="" odds="" of="" only="" outcome="" pertinent="" propensity="" prophylactic="" rate="" ratio="" re-arrest="" recurrent="" reduced="" s="" score-matched="" sensitivity="" span="" survival="" to="" vf="" was="" with="">
CONCLUSIONS:

Administration of prophylactic lidocaine upon ROSC after OHCA was consistently associated with less recurrent VF/VT arrest, and therapeutic equipoise for other measures. The prospect of a promising association between lidocaine prophylaxis and outcome, without evidence of harm, warrants further investigation.




Sympathectomy:

Lecture by Peter J. Schwartz
https://vimeo.com/145288008


http://www.nature.com/nrcardio/journal/v11/n6/abs/nrcardio.2014.19.html


Schwartz, PJ. Cutting Nerves and Saving Lives.  Heart Rhythm 6(6):760-763, 2009-06-01

Chest Pain, LBBB, and a ratio that does not quite meet the Modified Sgarbossa Criteria

Case

A 55 year old male heavy smoker presented with agonising chest pain and this ECG:
There is sinus rhythm.
There is left bundle branch block (LBBB)
There is no concordant ST elevation.
The highest ST/S ratio is in V3, at approximately 4.5/24 = 0.19
This is not a high ratio, but it is also not normal.

See this post:

A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia




The mean maximal ST/S ratio in non-ischemic LBBB is about 0.11.  So 0.19 (19%) is abnormal.

In our validation study of the Modified Sgarbossa Criteria for diagnosis of acute coronary occlusion, we found that it performed similarly well using a cutoff of 20% or 25%:

Sensitivity and Spec at 20%: 84% and 94%
Sensitivity and Spec at 25%L 80% and 99%

So at a ratio of 0.19, there is still a high probability of occlusion.

I was sent this ECG by Facebook messenger, and asked my interpretation.  Here is my response:

"V3 is suspicious for excessive discordance. I would say it does not look like an acute STEMI, but I could be wrong."

The patient received thrombolytic therapy.

An angiogram was done after thrombolysis:

It showed moderate diffuse coronary disease and no thrombus.
LAD: mid segment moderate disease
OM: mid segment moderate lesion.
OM2: ostial moderate lesion
Ramus: moderate mid segment lesion
RCA: diffuse disease mid to distal, moderate lesion

The angiogram was considered to be "negative" for a culprit.


An ECG was repeated:
LBBB is resolved.
There is T-wave inversion in V2 and V3 highly suggestive of Wellens' waves
This represents LAD reperfusion


An echo was done:

There were septal, apical, and anterior wall motion abnormalities.

Troponins
     --(high sensitivity troponin I BiomerieuxVIDAS TNHS):
99% reference = 19 ng/L (%CV = 7% at this level)
LoD = 2 ng/L

Initial: 13 ng/L (detectable, but still below the 99%)
Followup: 38 ng/L  (above the 99% and with a significant rise)

Here is the manufacturer's chart for interpretation:
You can see that a rise in high sensitivity troponin of greater than 10 ng/L is a "rule in."


Even with a "negative" angiogram, the weight of evidence heavily favors LAD occlusion at the time of the ECG:

1. There was excessive discordance, even if it did not meet the 20% or 25% cutoff
2. There was coronary disease, even if no thrombus; thrombus would likely be lysed by tPA
3. The followup ECG (most important) was consistent with reperfusion of the LAD
4. There were corresponding wall motion abnormalities.
5. The high sensitivity troponin had a diagnostic delta, even though the absolute level was minimally elevated

Learning points

1.  The cutpoints of 20% and 25% for the Modified Sgarbossa criteria maximize specificity, but are not fully sensitive for acute coronary occlusion.  Every case must be evaluated carefully.

2.  Not all ACS has a clearly visible culprit.

3.  The best way to assess whether ST elevation represents ischemia is to look at followup ECGs.  If the ST elevation resolves or evolves, then it is ischemic, even with all negative troponins!

See my last case:

Chest pain, ST elevation, and negative serial trops: normal variant ("early repol"). Right?

Chest pain, ST elevation, and negative serial trops: normal variant ("early repol"). Right?

Case


A 58 year old man presented with intermittent chest pain for 2 weeks. He has active pain at the time of this initial ECG:
QTc is 455 ms
What do you think?














Analysis

To me this is clearly an anterior STEMI, and it meets STEMI criteria even for someone under age 40 (at least 2.5 mm in V2 and V3, as measured at the J-point, relative to the PQ junction).

On the other hand, normal variant ST Elevation (often called early repolarization) may also have very marked ST elevation.   So when there is upward concavity in all of V5-V6, absence of any ST depression, and absence of Q-waves, it still might be early repol and the computer might not call this anterior STEMI.  Even the most contemporary algorithms are very inaccurate (see references below).


Thus, it is useful to use the STEMI-early repol calculator
(which is not, as far as I know, programmed into automated interpretation algorithms):

You can find the calculator here:
--- (http://hqmeded-ecg.blogspot.com/p/rules-equations.html)
--- Or use the free iPhone app ("subtleSTEMI):  https://itunes.apple.com/us/app/subtlestemi/id617146818?mt=8
---Or go to www.mdcalc.comhttps://www.mdcalc.com/subtle-anterior-stemi-calculator

The QTc = 455
ST Elevation at 60 ms after the J-point (STE60V3) = 4mm
R-wave amplitude in V4 (RAV4) = 17 mm

Formula value = 26.1.  At greater than 23.4, this is diagnostic of LAD occlusion until proven otherwise.

Clinical Course

The computer did not diagnose STEMI.  It did say "consider anterior injury."  However, the physicians thought it was early repolarization and admitted the patient for rule out MI.

Serial troponins were all undetectable (Beckman Coulter Access AccuTnI+3 Troponin I on DXL 600), LoD 0.010 ng/mL, 99% reference at 0.040 ng/mL), and thus the patient did rule out for MI.

At some point, the symptoms resolved; it is unclear when.

Fortunately, they recorded a second ECG 12 hours after the first:
Notice that all ST elevation has resolved!


The physicians were alarmed by this and realized they may have dodged a bullet.  They took the patient to the cath lab and found an 80% thrombotic LAD lesion.  It was stented.

This patient (and his physicians) were very lucky.  Had this patient not spontaneously reperfused, he would have lost his entire anterior wall, and possibly died.

It is dangerous to rely only on troponins for the diagnosis of acute coronary syndrome!


Learning Points:

1. Not all ischemic ST elevation results in elevated troponin
2. Unstable Angina still exists!!  Troponins may all be negative even with severe ACS.
3. Use the formula
4. Serial ECGs should be every 15 minutes, NOT every 12 hours!
5. High sensitivity troponins might have made a difference.  But maybe not.
6. Often, the only way to diagnose acute MI is with serial changes in the ECG.  In this case, resolution of ST elevation was diagnostic even in the absence of troponin elevation.



References

Contemporary computer algorithms are insensitive (65%) for STEMI, and only approximately 90% specific:

1. Mawri S, Michaels A, Gibbs J, et al. The Comparison of Physician to Computer Interpreted Electrocardiograms on ST-elevation Myocardial Infarction Door-to-balloon Times. Critical Pathways in Cardiology 2016;15:22-5.

2. Garvey JL, Zegre-Hemsey J, Gregg RE, Studnek JR. Electrocardiographic diagnosis of ST segment elevation myocardial infarction: An evaluation of three automated interpretation algorithms Journal of Electrocardiology 2016;49:728-32.


Inferior MI? Or LVH?

A middle-aged male presented with acute chest pain:
There is sinus rhythm.
There is LVH by voltage in aVL, with what may appear to be secondary repolarization abnormalities
(so-called "LVH with strain", but this is a misnomer because it implies ischemia.  "LVH with secondary repolarization abnormalities" is more appropriate).
It has the "hockey stick" morphology typical of LVH with secondary repolarization abnormalities.

What do you think?














Here is the ECG of another middle-aged male with acute chest pain:

It is similar, but notice how the T-waves are not nearly as proportionately large as in the above ECG.

What do you think?
















The bottom ECG is that patient's baseline LVH.

The top ECG is LVH with superimposed inferior acute MI.   The T-waves (both upright and negative ones) are far too large in proportion to the QRS.  There is also a concordant T-wave in lead II, and ischemic appearing biphasic T-waves in V4-V6, with a flattened ST segment in V3, all suggesting posterior and lateral involvement.

Technically, it is not "STEMI" because the ST elevation at the J-point is less than 1 mm.

This (top) ECG was missed by several interpreters and the patient had very delayed reperfusion therapy.  

The culprit was 100 % thrombotic occlusion of the mid RCA.  The peak troponin I was 47 ng/ml (very high).  There was a regional wall motion abnormality in the inferior and posterior walls.   The LAD was not involved.

The patient was discharged with a diagnosis of NonSTEMI.

There actually was a previous ECG for comparison, which proves the point.  Here it is:
Very different from LVH with superimposed inferior STEMI.


Here is the post-PCI ECG:
Notice inferior reperfusion (inverted) T-waves
Notice precordial large T-waves (posterior reperfusion T-waves)
Notice lateral reperfusion T-waves.
These are "Wellens' waves" of inferior, posterior, and lateral walls.


Learning point

Know the T-wave to QRS proportions in LVH vs. LVH with superimposed MI.

Patient with severe DKA, look at the ECG

This patient presented with severe DKA.

Here is the ECG:
Sinus tachycardia.
What do you think?




















The computer and physician reader wrote: "ST depression, consider subendocardial injury."
The computer read the QT as 365 ms and the QTc as 424 ms.  What else?

I read the QT interval as somewhere between 480 and 580 ms, depending on the complex, with a QTc (Bazett correction) of 630 - 763 ms.  There is a very prominent U-wave and some of what may appear to be a QT interval is a QU interval.  So the real QT is shorter, but the computer does not mention the U-wave, and the U-wave is as important as the T-wave in predicting cardiac dysrhythmias.

This is an extremely dangerous ECG.

The K returned at 1.9 mEq/L.

This is extremely low for DKA.

K in DKA is usually high from shifting out of cells, and will go lower as it shifts into cells during treatment.

Therefore, hypokalemia in the setting of DKA is truly life threatening and must be treated aggressively.

When the ECG shows the effects of hypokalemia, it is particularly dangerous.  In spite of aggressive K replacement, the patient went into ventricular fibrillation.


Discussion

See this post: STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes

I could find very little literature on the treatment of severe life-threatening hypokalemia.  There is particularly little on how to treat when the K is less than 2.0, and/or in the presence of acute MI.

Here are the American Heart Association Guidelines: 

Part 10.1: Life-Threatening Electrolyte Abnormalities

Treatment of Hypokalemia

"The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement.  IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5 mEq/L).  Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable.

"Administration of potassium may be empirical in emergent conditions.  When indicated, the maximum amount of IV potassium replacement should be 10 to 20 mEq/h with continuous ECG monitoring during infusion  A more concentrated solution of potassium may be infused if a central line is used, but the tip of the catheter used for the infusion should not extend into the right atrium.

"If cardiac arrest from hypokalemia is imminent (i.e., malignant ventricular arrhythmias are present), rapid replacement of potassium is required.  Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if needed.  Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia."

CASE: Prehospital Cardiac Arrest due to Hypokalemia

I recently had a case of prehospital cardiac arrest that turned out to be due to hypokalemia.
We could not resuscitate her, but we did have excellent perfusion with LUCAS CPR, such that pulse oximetry had excellent waveform and 100% saturations, end tidal CO2 was 35, and cerebral perfusion monitoring was near normal throughout the attempted resuscitation.

During the resuscitation, I ordered 10 mEq KCl push, but the patient received 40 mEq of KCl, push (far more than recommended)  The resident had ordered 40 mEq and that is what the nurses heard.

Is 40 mEq too much? Or the right amount?

Contrary to my expectations, after pushing 40 mEq, the K only went up to 4.2 mEq/L.


What is the right amount of K to push in life-threatening hypoK?
In a 70 kg person, there are 5 liters of blood and 3 liters of serum.  Since it takes some time (how long?) for K to shift out of the intravascular space into the interstitial space and then into the intracellular space, 3.0 mEq of K pushed fast and circulated theoretically would raise serum K immediately by 1.0 mEq/L, and 10 mEq would increase it by 3.3 mEq/L, from 1.9 to 5.2.   Thus, 40 mEq should raise it by 13 mEq/L!! 

But this is before redistribution to the interstitial space.

As I indicated above, in our cardiac arrest case, after pushing 40 mEq, the K only went up to 4.2 mEq/L.   
  
There are about 13 liters of extracellular fluid in a 70 kg person (10 liters interstitial fluid + 3 liters serum).  So if K redistributes very quickly to this extracellular space, then 40 mEq is appropriate.

The difficulty is in estimating the ongoing shift.  As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly.  Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.

Total Body Potassium: a 70 kg person has about 7500 mEq of total body K, but the extracellular fluid has only about 45 mEq!   Of course the difficulty with K replenishment is that the total body stores may be depleted by far more than can possibly be quickly repleted.  The estimated deficit associated with a serum decrease from 4.0 mEq/L to 3.0 mEq/L is 100-200 mEq of total body K, and from 3.0 mEq/L to 2.0 mEq/L, the associated loss is double, at 200-400 mEq.* [Sterns RH, et al. Internal potassium balance and the control of the plasma potassium concentration. Medicine (Baltimore) 1981;60:339-54].  

But 100 mEq given all at once by bolus, could (before any redistribution to interstitial space) raise the serum K by 33 mEq/L (and be immediately fatal)!!

*The NEJM review referenced below (and ACLS, for what that is worth), states that, on average, in a "typical" 70 kg person, the serum K falls by 0.3 mEq/L for every 100 mEq total body deficit.  However, this review references the Sterns article above, which by my reading does not state this.

Further complicating the issue is that severe hypokalemia can result in rhabdomyolysis and subsequent K release, with resulting hyperkalemia!

Here is review of hypokalemia from the NEJM, but it is mostly about etiology, and says little about rapid replacement in life-threatening hypokalemia EXCEPT to emphasize how dangerous rapid replacement is.