Smartphone electrocardiograms reveal painful left bundle branch block syndrome and illustrate associated electrophysiological phenomena

EP Europace Painfull LBBB syndrome 

A 69-year-old lady presented with exertional chest discomfort. A 12-lead ECG indicated anteroseptal T wave inversion (TWI) (Panel A, left), suspicious for Wellens’ syndrome. However, cardiac catheterization (Panel A, right) and echocardiography were normal. Her symptoms persisted and she purchased a smartphone electrocardiogram (EGM) device (AliveCor KardiaMobile™, USA). Recordings revealed that her pain coincided with the sudden onset and resolution of left bundle branch block (LBBB) (Panel B, top EGM). ‘Painful LBBB Syndrome’ is an increasingly recognized entity and is easily missed following a reassuring ischaemic evaluation. These single lead recordings also illustrate associated electrophysiological phenomena. The LBBB is rate related (Panel B, top EGM), suggesting a phase 3 block. Resolution occurs at a lower rate than onset, due to ‘linking phenomenon’ whereby concealed retrograde invasion of the bundle occurs from the contralateral side. Premature ventricular contractions allowed time for the LBBB to recover (Panel B, middle), consistent with aforementioned explanations for ‘functional’ block. The TWI was also demonstrated on the KardiaMobile™ by recording an anterior precordial lead (Panel B, bottom). Known as ‘cardiac memory’, TWI transiently occurs after a period of abnormal ventricular activation.

In summary, smartphone-based EGM’s continue to improve our diagnostic capability and can illustrate complex electrophysiological phenomena

Painful left bundle branch block syndrome: Clinical and electrocardiographic features and further directions for evaluation and treatment- Heart Rhythm Society 

Narrow QRS tachycardia ("SVT") in the ICU

Supraventricular tachycardias should be described as long RP or short RP tachycardia.

SVT is a general term and has no reference to the underlying pathophysiology or mechanism causing narrow QRS tachycardia. Short RP tachycardias, are most commonly seen in clinical practice,  long RP tachycardias to a lesser extent  (the latter more frequently in  the ICU setting)
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One should always look at the initiation of the tachycardia, i.e. is there warm up or ramp-up phase.  How does the tachycardia terminate:  is there a P before conversion to sinus tachycardia after administration of adenosine, or does the tachycardia terminate without a P-wave?  What is the axis of the P-wave during narrow QRS tachycardia, i.e. is axis inferior or superior?

Adenosine should always be administered both as a diagnostic and possible therapeutic agent in the setting of sudden onset hemodynamically stable narrow QRS tachycardia ( and regular monomorphic VT- see below) . Adenosine terminates close to 100% of short RP ( narrow QRS) tachycardias (slow-fast AVNRT as most common rhythm).

Long RP (narrowQRS)  tachycardia's are seen less common but deserve some further attention (higher incidence in the ICU setting) :

1.  Fast-slow AV nodal  reentry tachycardia
2.  AV reentry tachycardia with retrograde conduction over accessory pathway
3.  Ectopic atrial tachycardia/focal atrial tachycardia
4.  Sinus tachycardia

Adenosine will terminate AV nodal reentry tachycardia, but very uncommonly there is an adenosine sensitive accessory pathway.  It will not terminate sinus tachycardia but can cause slowing of the rate.
However, some ectopic atrial tachycardias can be terminated by adenosine.(60-80%)

Of note, adenosine can also be administered for hemodynamically stable regular monomorphic wide complex QRS tachycardia, as it will break AV reentry tachycardia with antegrade conduction over accessory pathway as well as some forms of ventricular tachycardia

The new ACLS guidelines now has adenosine given up to 2 times instead of 3 times.  The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 cc normal saline bolus ( use 3 -way stopcock).  If the patient's rhythm does not convert within 1 to 2 minutes,  a second 12 mg dose may be given similar fashion.

A lower initial dose of 3 mg should be used in patients taking dipyridamole or carbamazepine as these 2 medications potentiate the effect of adenosine.

Also, prolonged asystole has been seen with the use of normal doses of adenosine in heart transplant patients and central line use.  Therefore, the lower, 3 mg dose should be considered for patient's with a central venous line or history of heart transplant

Sometimes termination is followed by an immediate return of the tachycardia,  even in AVNRT. In these patients, intravenous verapamil 5-10 mg slow push can be used.  Diltiazem, 20 mg IV as a loading dose followed by 10 mg/min continuous infusion, can be used but is less effective than verapamil.  Intravenous beta blockers i.e. metoprolol, esmolol, can be used as an alternative to verapamil or diltiazem in patients who do not not convert with or are intolerant to adenosine.

This case report in the New England Journal of Medicine is an interesting presentation of focal atrial tachycardia secondary to  hyperthyroidism ( Graves' disease). 
It also highlights that performing contrast studies will cause temporary suppression of  thyroid production due to administration of a high iodine load and " masque" hyperthyroidism for certain period of time.

Cardiac Amyloidosis: Not a Rare Disease Anymore

1. Transthyretin amyloid cardiomyopathy is a life-threatening, progressive disease that is often underdiagnosed and misdiagnosed
2. Certain clinical scenarios have been identified that now warrants screening for transthyretin amyloid cardiomyopathy
3. Once transthyretin cardiomyopathy suspected definitive diagnosis can usually be achieved noninvasively
4. Accurate, early diagnosis of transthyretin cardiomyopathy ischemic to enabling appropriate patient care

screening for transthyretinamyloid cardiomyopathy in everyday practice, published in JACC HF failure, July 2019

Journal of the American College of cardiology state-of-the-art review:
transthyretin amyloid cardiomyopathy


The following Webinar from  the European Society of  Cardiology  ( ESC) which gives a good overview about the diagnosis and treatment various forms of cardiac amyloidosis, presenting several case reports

The EACVI Webinar : Diastolic function made easy: tips and tricks for daily practice is today!

E/A and E/e' to Assess Diastolic Dysfunction and LV Filling Pressures
JACC VOL. 69, NO. 11, 2017

Association of Mineralocorticoid Receptor Antagonist Use With All-Cause Mortality and Hospital Readmission in Older Adults With Acute Decompensated Heart Failure

Use of MRA at discharge from ADHF  ( acute decompensated heart failure in HFrEF/HFpEF) hospitalization appeared to be associated with a lower risk of heart failure hospitalization but not with lower all-cause mortality or overall rate of hospitalization. No in this end- point was seen  benefit in 94% of patients with average age of 80 years old .

These findings suggest that MRA use might be associated with minimal, if any, clinical advantage. Further studies appear to be needed to identify the patient groups that may find value in MRA treatment and for findings to be confirmed by RCTs in patients hospitalized for ADHF.

This reminds me of the digoxin story in HF patients - high risk medication with essentially no benefit . Another med to de-escalate elderly patients often complicated HF medication list .

Tako-tsubo Cardiomyopathy and its multiple variants

Tako - Tsubo Cardiomyopathy

The correct answer is a Tako-Tsubo Cardiomyopathy. [Stress cardiomyopathy or broken heart syndrome]. Typical presentation is a patient with chest pain after emotional distress and EKG presentation suggestive of an ST elevation myocardial infarction.[ST elevation]



ST elevation myocardial infarction is not entirely an incorrect answer. The patient still is treated initially as a STEMI, but then in the catheterization laboratory the usual findings are no significant obstructive coronary artery disease with typical ballooning of the apex of the heart on left ventriculogram. Therefore the syndrome was also called apical ballooning syndrome or Octopus trap syndrome, first described in the mid 1980s by a Japanese scientist

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However more recently several variants have been noted, one variant is where there is akinesis of the mid ventricle and hypercontractility of the apex and the base [see article] and yet another form is reversed Tako-Tsubo syndrome, or also called “squid syndrome”. This gives an image on ventriculogram and echocardiogram with apical hypercontractility and basilar akinesis




There are specific ECG criteria that differentiates Tako-Tsubo Cardiomyopathy from a true STEMI secondary to plaque rupture or type I myocardial infarction.



Although this EKG looks like an ST elevation myocardial infarction , the distribution of the ST segment elevation is unusual as well as the shape of the ST segments. There is also no reciprocal ST segment depression. The frontal axis is typically shifted more leftward.

The EKG at first glance can also look like pericarditis, but the history is not compatible with this and although there are a few leads with what appears to be PR depression there is no PR elevation in aVR and is also no ST elevation in all leads and/or T wave inversion. Squid syndrome ( reverse tako -tsubo syndrome) presents with ST depression and QTC prolongation. No J wave's are seen which would be associated with hypothermia, hypercalcemia, idiopathic VT or even Brugada syndrome.



The point of this question is to alert you that when elderly people complain of a "bad dream" or go through emotional/physical distress and then develop chest pain, and particularly when they complain of associated shortness of breath either at rest or on exertion, always keep this syndrome and its multiple variants in mind. Call EMS and get an EKG in the interim if you can, and if not one available call EMS and refer the patient to the hospital. Often the patient will minimize her/his symptoms and and will say "it's nothing and just felt bad".There is no reason to remember all the criteria and EKG features, as the answer lies in the patient's history. Often this is a benign syndrome but not always.Also this patient has 3+ ( on a scale of 4) mitral regurgitation and likely presented with crackles and left sided heart failure symptoms. The other video I attached is a NC female school bus driver , who ended up in a ditch and some of the kids were hurt . She was emotionally so shaken she developed also a stress cardiomyopathy

Attached articles

Here is the distribution of the answers of the initial 25 answers.

Lung ultrasound for the diagnosis of weaning-induced pulmonary oedema

Weaning-Induced Pulmonary Oedema (WIPO) is a common cause of failure of weaning from mechanical ventilation. The change in heart-lung interactions during Spontaneous Breathing Trials (SBT) can lead to WIPO, which can be detected by pulmonary artery occlusion pressure, left ventricular filling pressure, or extravascular lung water. Detection of multiple B lines by lung ultrasound may used to detect WIPO.

To test this hypothesis, a mixed population of ICU patients was enrolled. B-lines were counted in a rib short-axis scan at four points on the anterior chest. WIPO was diagnosed a posteriori by two experts using several criteria.

43 patients were included in the cohort, who had 27% WIPO overall and 52% WIPO in patients with failed SBT. The best accuracy to diagnose WIPO was reached when delta B lines were ≥6, with 88% sensitivity and 91% specificity, and with 79% of PPV. Accuracy was similar when considering only failed SBT trials.

The authors conclude that WIPO has a high incidence in mixed population of ICU patients, and that lung ultrasound may be used to diagnose WIPO with high accuracy using a cut-off of ≥6 B-lines counted on the anterior chest.

TAKE HOME MESSAGE

WIPO is a frequent complication of weaning from mechanical ventilation.Lung Ultrasound may be used to detect WIPO with high accuracy, when the number of B-lines on the anterior chest increases by ≥6.

REFERENCES

1) Ferré A, Guillot M, Lichtenstein D, Mezière G, Richard C, Teboul JL, Monnet X, Lung ultrasound allows the diagnosis of weaning-induced pulmonary oedema. Intensive Care Med. 2019 May;45(5):601-608. doi: 10.1007/s00134-019-05573-6. Epub 2019 Mar 12. PubMed PMID: 30863935.