POTD: Shock to the heart (and you're to blame)

Hello folks,

Today’s POTD will be a quick overview of implantable cardioverter-defibrillators (ICDs) and their common complications.

Why do patients have an ICD in place?

Secondary prevention in previous episodes of unstable VT or VF.

Primary prevention if pt has hx of severe heart failure or underlying congenital arrhythmias.

Exact indications listed below:

Hx of MI within last 40 days with LVEF of <30%, NYHA Class II or III heart failure with an LVEF <35%, underlying disorders which place them at high risk of unstable VT or VF such as congenital long QT syndrome, HOCM, Brugada, ARVD

What does an ICD do?

Note that all ICDs are also pacemakers, but the reverse is not true (pacemakers do not have defibrillator/shocking functionalities).

Anti-tachycardia function: If the patient is tachycardic above a pre-set range (usually 150-220) the ICD will compare QRS morphology to a known sinus beat and if determined to be different, will deliver a series of paced beats at a rate slightly faster than the native rate to break the re-entrant cycle.

Defibrillation in response to sensed VT or VF

What can go wrong with ICDs?

In short, problems with ICDs/pacemakers come down to a failure of sensing or a failure of pacing.

Pacing malfunction:

Failure to pace: pacemaker doesn’t deliver a stimulus at all, resulting in return of the underlying rhythm.

Failure to capture: pacemaker delivers a stimulus, but the stimulus does not result in depolarization. EKG will show pacer spikes that are not followed by P waves or QRS complexes. 

Sensing malfunction:

Failure of sensing: pacemaker fails to sense normal cardiac activity so an impulse is delivered inappropriately. EKG will show intermittent pacer spikes.

Oversensing: pacemaker identifies external signals such as from skeletal muscle contraction as “appropriate” and will not send an impulse when one is required.

Other problems:

Pacemaker mediated tachycardia: formation of a re-entrant circuit from retrograde p waves being sensed as native atrial activity, causing inappropriate tachycardia. This tachycardia does not exceed the programmed upper limit of the ICD.

Twiddler syndrome: accidental or intentional manipulation of the pulse generator resulting in dislodgement of pacing leads resulting in sx such as diaphragmatic or brachial plexus pacing. Will manifest as arm twitching or uncontrollable hiccups depending on where lead has migrated.

Miscellaneous pearls

• Because most ICDs have only a lead in the RV, a LBBB pattern is expected on EKG; new RBBB pattern/axis deviation may indicate lead migration/dysfunction.

• If you need to externally cardiovert or defibrillate, place pads at least 8cm away from device in anterior-posterior orientation.

• Placing a magnet over the device will remove the defibrillator function of an ICD, but pacing function will be kept. This will be helpful in the setting of inappropriate shocks. Kept in charge nurse desk on north side usually!

• Every patient should carry a pocket card indicating the manufacturer of their ICD, but it can also be ID’d by CXR and using an app called Pacemaker!

• We’re lucky we have electrophysiology as a consult service here at Maimo that can interrogate a device for us, but each company has on-call representatives that will come interrogate a device 24/7.

  • Medtronic Inc. (1-800-328-2518)

  • St. Jude Medical Inc.(1-800-722-3774)

  • Boston Scientific Inc. (1-800-227-3422)

References

https://www.emdocs.net/ecg-pointers-icds-and-when-they-malfunction/

https://www.emdocs.net/em3am-pacemaker-aicd-complications/

https://www.emdocs.net/pacemaker-and-aicd-management-in-the-emergency-department/

https://rebelem.com/pacemaker-basics/

https://coreem.net/procedures/how-to-use-a-magnet/

https://litfl.com/pacemaker-malfunction-ecg-library/

Differential for ST Elevation

The differential for ST elevation is broader than ACS (although it would be nice if medicine were that easy). In EM, the maxim is always to think about the worst first. After you have determined the patient is likely not experiencing an acute coronary occlusion aka ST-Elevation Myocardial Infarction, what else could lead to ST elevation? Outside of acute coronary occlusion, there are also a few causes that are not so benign. 

Hyperkalemia can be a cause of ST elevation, but distinguishing features include peaked T waves, widened QRS complexes, and decreased P wave amplitude. 

Another dangerous cause of ST elevation is Brugada syndrome, where ST elevation is most prominent in V1-V3 and is accompanied by T wave inversions. 

Chronic causes of ST elevation include Left Ventricular Hypertrophy, LBBB, & LV aneurysm. Of course, you could have an acute coronary occlusion leading to STEMI in patients who have baseline LVH, LBBB, or LV aneurysm. This is out of scope from this POTD, but modified Sgarbossa's criteria seeks to help identify STEMIs in patients who have underlying LBBB (or paced rhythms). 

LV aneurysm morphology often has deep Q waves with persistent ST elevation and T wave inversions and is accompanied by anatomical aneurysms that can be visualized on echocardiogram.

LBBB is characterized by a wide QRS with dominant S wave in V1 and a broad notched R wave in V6. 

There are many criterias for LVH, but morphology wise, ST elevations in LVH are usually confined to V1-V3. There can also be ST depressions in the lateral leads.

Two final causes of ST elevation include Benign Early Repolarization (BER) and pericarditis. These can often be tricky to distinguish from subtle STEMIs, especially subtle anterior STEMIs. 

Classically in pericarditis, there is PR depression, diffuse ST elevation (without ST depressions), and ST elevation in lead II > lead III. In BER, there is again diffuse ST elevation without ST depressions, elevations are often most prominent V2-V5, and there can be J point notching. 

Picture below showing some common causes of ST elevation

Sources:

https://litfl.com/left-ventricular-hypertrophy-lvh-ecg-library/

https://emergencymedicinecases.com/ecg-cases-st-elevations-mnemonic-occlusion-mi/

https://litfl.com/left-bundle-branch-block-lbbb-ecg-library/

http://hqmeded-ecg.blogspot.com/2020/07/subtle-ecg-findings-of-left-anterior.html

Wellens Syndrome & Pseudo-normalization

So Wellens syndrome is a STEMI equivalent right? That is part of it, but not the whole picture. When we say STEMI or STEMI-equivalent, the image of a fully occluded coronary artery that requires immediate PCI comes to mind. Wellens syndrome is not really a “STEMI” but more of a post-STEMI or a pre-STEMI (along with being a non-STEMI). I’ll explain why.

First we will review Wellens syndrome and then we’ll go into what it represents. Symptoms usually include resolved angina, either spontaneously or after treatment (nitro, aspirin). The troponin will be negative or minimally elevated & the EKG will not show signs of irreversible ischemia such as deep Q waves or poor R wave progressions. Lastly, you’ll see T-Wave Inversions in the anterior leads. There are two types of Wellens waves, pictured below and they occur when chest pain is resolved. Resolved chest pain means the artery has spontaneously reopened and the myocardium is being perfused. Thus Wellens waves are reperfusion waves, rather than waves that represent an acute coronary occlusion. 

However, if these patients do not receive PCI at some point, they are at high risk for large anterior MI due to near occlusion of the LAD. 

The phenomenon of pseudonormalization also occurs in Wellens syndrome, further making it easy to accidentally discharge these patients. In pseudonormalization, recurrence of chest pain results in normalization of T waves and elevation of ST segments. When the T waves are inverted, the artery is open (albeit barely) because the T waves represent reperfusion. When the patient develops chest pain (since the artery has fully closed), the T waves flip on their way to becoming hyperacute T waves. Catching an EKG at this unfortunate time could deceive you into thinking the patient has a “normal” EKG 

This nearly occluded lesion is classically associated with LAD and thus usually seen in the anterior leads. However, a 99% coronary lesion and thus occlusion/reperfusion phenomenon known as Wellens can occur in any coronary artery. For example, you'll see Wellens in the inferior leads for RCA lesions that spontaneously reopen. 

While resolved symptoms and EKG signs of reperfusion don’t require immediate cath lab activation, post-ischemic TWI require aggressive treatment while waiting for PCI. These are the highest risk NSTEMIs! Include these findings in your signouts. Be on the lookout for return of chest pain, which points towards acute reocclusion & do not be fooled by pseudonormalization. Also patients who have TWI and active CP are patients with typical ACS/NSTEMI, not necessarily Wellens/99% coronary artery occlusion. 

Wellens is a normal reassuring finding post cath lab since it means the interventionalist has successfully reperfused the coronary. It is scary in the ED because it was spontaneous reopening, which could mean an entire wall of the LV is only being supplied by an artery that is 1% open.