From Missed Hemodialysis to Multiple Arrhythmias

November 2, 2020October 23, 2020 ~ Gayatri Lekshmi Madhavan, India ~ 2 Comments

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern.

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters.

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
What was the necessity for carrying out SLED for this patient?
Why was this patient not immediately cardioverted in the ER?
If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

Cite this article as: Gayatri Lekshmi Madhavan, India, "From Missed Hemodialysis to Multiple Arrhythmias," in International Emergency Medicine Education Project, November 2, 2020, https://iem-student.org/2020/11/02/missed-hemodialysis/, date accessed: June 1, 2023

The EKG Case of No Symptoms

October 26, 2020October 23, 2020 ~ Anthony Rodigin, USA ~ Leave a comment

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

Anthony Rodigin Tweet

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely.

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle.

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus.

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output.

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in.

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter.

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels.

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse.

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event:

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

Cite this article as: Anthony Rodigin, USA, "The EKG Case of No Symptoms," in International Emergency Medicine Education Project, October 26, 2020, https://iem-student.org/2020/10/26/the-ekg-case-of-no-symptoms/, date accessed: June 1, 2023