A 69-year-old male patient presented to ED with bradycardia, hypotension, and looked unwell.
There was no available past medical history at the presentation.
This was his ECG now,
What is your diagnosis & how will you manage this?
Let's analyze the ECG:
This case will be a good one to discuss for many reasons:
1) It is a common life-threatening problem.
2) It is treatable.
3) It will give us the chance to discuss the condition diagnostically & therapeutically.
The ECG above shows the following features:
The rate is very slow (Bradycardia).
Very broad QRS complexes.
Irregular.
No clear P waves.
Hyperacute (Very big) T waves.
Sine waves.
When you combine the above, the answer will be easy for you.
Answer:
This was a case of Hyperkalemia, with a K level of 10.5 mmol/L.
Discussion:
Let me make it clear in the beginning that hyper K can cause any changes in the ECG, but the common changes are (Assess the P, PR, QRS, ST, T, in order):
1) lost or flat P wave.
2) Prolonged PR interval.
3) Wide QRS complex.
4) Can mimic VT (the above changes + tachycardia)
5) ST segment changes (especially ST elevation in V1-2).
6) Hyperacute T wave.
7) Rhythm changes (tachycardia, AV block, etc).
8) Pseudo ACS (new LBBB pattern, ST elevation).
9) Sine wave.
This is an ECG for another patient showing most of the signs of hyper K:
Another example of sine waves with K 8.2 mmol/L:
Another example with a K of 8.5 mmol/L:
An example of hyper K (K level was 7.8 mmol/L) mimicking VT (broad complex - regular tachycardia - no P waves - hyperacute T waves):
If this patient was treated by mistake as VT, the VT treatment can result in death!
This case was treated with only hyper K treatment and this was the repeat ECG of the same patient
This was the diagnosis part from the ECG side, next, we will talk about the management of the condition.
Management:
The 1st line of treatment for the above case should be IV Ca, but the question is: In which form, and with which dose?
There are 2 forms of IV Ca, Ca gluconate & Ca Chloride.
Ca Chloride:
Pros,
1) 3 times more potent than Ca gluconate (Ca Chloride dose is 10 ml of the 10% concentration).
2) Doesn't need the liver to be activated (can be given to severe liver failure).
Cons,
Irritant to veins & it causes severe vasoconstriction with extravasation, so it needs to go through a central line or a wide proximal peripheral cannula.
Ca Gluconate:
Pros,
Less irritant to veins than Ca Chloride, so safer to give via a peripheral cannula.
Cons,
1) Weaker than Ca Chloride, so to achieve the same effect of Ca Chloride with Ca Gluconate, you need triple the dose.
So, if you want to treat the above patient, the IV Ca dose should be Ca chloride 10% 10 ml, OR Ca gluconate 10% 30 ml.
2) Ca Gluconate must be hepatically metabolized before its associated calcium becomes bio-available, so in the setting of hemodynamic instability or poor liver function, such as cardiac arrest or patients with liver failure, it is preferable to use calcium chloride (theoretical risk).
You can repeat IV Ca once after 5 minutes, & this should buy you enough time for the other measures to work.
The 2nd line of treatment is B2 agonist nebulizer:
Salbutamol nebulizer with a dose of 10-20 mg.
The 3rd line of treatment is Glucose + Insulin:
Give 25 gm of Glucose + 10 units of soluble insulin IV over 15 minutes.
The 4th line of treatment is NaHCO3:
Regarding Na HCO3, it is only recommended by the Resuscitation Council UK in the peri-arrest situation with severe acidosis or renal failure.
This is a very nice Algorithm from the Resuscitation Council UK that summarizes the treatment of hyper K (There is a newer version from this, but I personally prefer this one):
Back to our patient:
This patient presented to ED in a peri-arrest situation with the ECG shown above, found to have a K 10.5mmol/L. All treatment of hyper K was given but unfortunately, he had a cardiac arrest & the team failed to gain ROSC even with all the above measures.
References & further readings:
I hope you find this useful.
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