A 78-year-old lady with long-standing hypertension on amlodipine was brought into hospital after seemingly 'passing-out' at home earlier in the day. This happened suddenly and without warning. She endorsed palpitations a few minutes prior to fainting. These palpitations have apparently been troubling her for months now and she's waiting to be seen by a cardiologist. In the ED, she's conscious and oriented x 3. BP was 110/64 mmHg, She had a rapid pulse rate of 178/min. She's diaphoretic but her cardiovascular examination was otherwise unremarkable. A 12-lead ECG was obtained and shown as below
Her laboratory investigations (sent from triage) were all within normal limits. c-Tn-T was 13 ng/L, serum K+ was 4.3 mmol/L.
Part (1) of this case
[1] what does the ECG show? what is the diagnosis/differential diagnosis?
[2] how would you manage the patient at this stage?
The following is a general framework to approach such arrhythmias. This is also the recommended algorithmic approach by the ACC/AHA and ESC guidelines on the diagnosis and management of supraventricular tachyarrythmias.
The 12-lead ECG in our patient shows the following findings:
- An irregular (irregularly irregular) narrow complex tachycardia (the QRS duration is hardly 1-1.5 small boxes wide; that is 40-60 msec).
- The QRS axis is deviated to the right. This is likely due to LPHB in an elderly, hypertensive lady who likely has ‘early’ degenerative conduction system disease. This is obviously a diagnosis of exclusion (but there don’t appear to be any other features in the ECG to explain the RAD e.g. RVH … etc)
- Incomplete RBBB
- There are wide-spread ST segment abnormalities. One can argue that the ST depression in seen in V1-V3 are due to RBBB. However, remember we mentioned earlier that the delayed conduction down the RBB is incomplete, and therefore unlikely to result in significant ST-T wave abnormalities. There is ST elevation in aVR and V1 and ST depression in II, III, aVF and V2-V6. These findings are consistent with diffuse subendocardial ischemia. This could be due to severe coronary artery disease (e.g. severe LM disease, triple vessel disease … etc) or due to non-coronary causes of global myocardial ischemia e.g. severe hypotension, severe hypoxia … etc. In this case, the elderly, postmenopausal lady is also hypertensive and likely has underlying coronary artery disease. Alternatively, she likely has concentric LVH from long-standing hypertension and the rapid ventricular rate from the irregularly rhythm resulted in (1) loss of much needed atrial contribution to forward cardiac output (can be as significant as 30-40% of the forward SV) (2) rapid ventricular rate and shortened diastole compromises myocardial coronary blood flow, which happens mainly in diastole (LV coronary perfusion mechanics).
- It is imperative to correct the QT interval for HR variability. Various equations have been suggested but all have their inherent limitations. The Bazzett’s formula for example tends to overcorrect at faster rates and undercorrects at lower rates.
The ECG is not consistent with a pre-excited arrhythmia as no delta waves are seen (unlike what is stated in some of the responses). Pre-excited AF would look like the tracing below. The diagram also summarizes the features characterizing the life-threatening arrhythmia.
Therefore, to answer the questions in this post:
1. The ECG shows an irregular narrow complex tachycardia with incomplete right bundle branch block, right axis deviation (likely due to LPHB), and diffuse subendocardial ischemia. The differential diagnosis for the irregular narrow complex tachycardia is:
a. AF (most likely)
b. Atrial flutter with variable AV block
c. Atrial tachycardia with variable AV block
d. Multifocal atrial tachycardia which is unlikely given
i. No predisposing conditions (COPD, theophylline intake … etc)
ii. There is no P wave before every QRS complex
2. Management would include:
a. ABC – make sure the patient is under continuous ECG monitoring
b. Obtain a BP recording in both arms
c. Consider pharmacological rate control. Options would include:
i. IV metoprolol
ii. IV diltiazem or verapamil
iii. IV adenosine: the response to adenosine can sometimes break the arrhythmias and declare the exact type as shown in the diagram below. The response in AVNRT and AVRT will be discussed in subsequent ECG cases.
d. Continuous ECG monitoring while administering the medications to understand the behavior of the arrhythmia (response to pharmacological agents and pattern of termination).
e. Carefully evaluate the post conversion ECG (if conversion was successful)
f. Serial ECG(s) and c-Tn-T ( I suppose that is reasonable given the worrisome ECG findings in an elderly lady with risk factors for CAD).
Stay tuned for Part (2) of this case. It is where all the action took place !!