< Brief History >
A 68-year-old man was admitted to the intensive care unit
(ICU) because of a witnessed collapse of sudden onset while he
was waiting for excision of a lipoma on his right elbow in
this hospital. He had had a history of hypertension for 10
years that had been treated with trichlormethiazide 1mg qd. He
had an established diagnosis of chronic obstructive pulmonary
disease (COPD) and reported having experienced brief episodes
of lightheadedness without warning. This lightheadedness
occurred occasionally, without any identifiable precipitating
factor, and it abated without intervention. In addition, he
had experienced episodes of shortness of breath on exertion,
which he attributed to a long history of cigarette smoking. He
had been otherwise healthy without having had any symptoms of
nausea, vomiting, chest pain and pressure sensation,
palpitations, diaphoresis, or syncope. He had no known family
history of heart disease or diabetes mellitus.
On physical examination, he was in no acute distress and
his consciousness was clear and oriented. He was afebrile, and
the blood pressure was 134/76 mm Hg, the pulse rate 65 beats
per minute, and the respirations 16 breaths per minute. The
oxygen saturation was 93% while he was breathing ambient air.
The neck examination showed no jugular venous distension or
carotid bruits. Auscultation of his chest revealed distant
breath sounds with no wheezing, crackles, or rhonchi. Cardiac
examination revealed a regular heart rhythm, with frequent
skipped beats and slightly accentuated second heart sounds.
There were no murmurs, rubs, or gallops. No peripheral edema
of the lower extremities was observed and the remainder of the
physical examination was normal.
An electrocardiogram (ECG) and a panel
of preoperative blood tests were ordered. The patient
experienced an episode of severe lightheadedness while waiting
for the operation. He became unconscious with a blood pressure
of 84/48 mm Hg. An ECG was recorded (Figures 1
and
2
).
< Laboratory data >
CBC/DC: (Time: 11:04am, June 26th, 2008, after
collapse)
WBC /μL |
8400 |
Band % |
0 |
RBC M/μL |
3.36 |
Seg % |
84 |
Hb g/dL |
13.2 |
Lym % |
4 |
Hct % |
39.6 |
Mono % |
6 |
MCV fl |
90.3 |
Eos % |
1 |
PLT. /μL |
326000 |
Baso % |
5.0 |
Biochemistry:
(Time: 11:04am, June 26th, 2008, after
collapse)
Alb
g/dL |
4.1 |
T-Bil mg/dL |
0.7 |
BUN
mg/dL |
25 |
K
mmol/L |
4.7 |
Cre mg/dL |
0.8 |
ALT U/L |
24 |
Glucose mg/dL |
116 |
Cla
mmol/L |
104 |
Na mmol/L |
135 |
AST U/L |
26 |
Mg mmol/L |
1.1 |
Ca
mmol/L |
8.2 |
Serial cardiac enzyme (after collapse)
|
11:04am 06/26/2008 |
3:15m 06/26/2008 |
9:12pm 06/26/2008 |
3:24am 06/27/2008 |
9:25am 06/27/2008 |
CK(U/L) |
180 |
198 |
194 |
190 |
188 |
CK-MB(U/L) |
8 |
12 |
10 |
8 |
12 |
Troponin-I
(U/L) |
0.08 |
0.02 |
0.04 |
0.08 |
0.04
|
Artery blood gas (10:28am, 06/26/2008, after
collapse) : pH: 7.38, PaCO2: 48.3, PO2: 60, HCO3-:
25.6
CXR: Normal heart size and clear lung
fields.
Echocardiography (11:28am, 06/26/2008, after
collapse): normal size of the left atria (LA) and
left ventricles (LV) with good contractility; mild TR and mild
pulmonary hypertension.
Magnetic resonance imaging of the heart (8am,
06/27/2008, after collapse): normal LV and RV
structures and systolic function.
< Course and Treatment
>
A 200-J biphasic cardioversion shock was performed and the
patient regained consciousness with blood pressure returning
to 110/62 mm Hg. The patient was transferred to ICU. Sotalol
(320 mg/day) and atenolol (100 mg/day) were administered. The
follow-up ECG were normal, and his serial examinations of
cardiac enzymes as well as serum electrolytes were within the
normal ranges for the next 24 hours during the ICU stay. A
coronary angiogram revealed patent coronary arteries. An
electrophysiological study demonstrated an arrhythmogenic
focus of myocardial irritability, which was thought to be
caused by scar tissue from a previously unrecognized
myocardial infarction, was identified. An automatic internal
cardiac defibrillator was placed and, subsequently, his lipoma
on the right elbow was successfully excised.
< Case Discussion >
A wide-complex tachycardia is a
form of cardiac dysrhythmia that originates from either a
ventricular focus or a supraventricular focus associated with
a conduction abnormality and presents with a ventricular rate
that exceeds 100 bpm in the setting of a QRS duration greater
than or equal to 120 milliseconds. In this case, a 12-leads
ECG showed that the ventricular rate was greater than 100 bpm
and the QRS duration was greater than 140 milliseconds with no
regular P waves.
Ventricular tachycardia (VT)
accounts for up to 80% of wide-complex tachycardias, which may
be higher in patients with structural or ischemic heart
disease. VT also occurs in patients with hypoxemia, acidemia
and electrolyte abnormalities, such as hypokalemia and
hypomagnesemia, as well as in patients with mitral valve
prolapse and receipt of drugs that may prolong the QT
interval, such as digitalis, antihistamine, tricyclic
antidepressants. VT occasionally occurs in individuals without
any identifiable risk factors.
Symptoms associated with a
wide-complex tachycardia are typically caused conditions that
result in a decreased cardiac output, namely presyncope,
syncope, orthostasis, exercise limitation, dyspnea, and
hypotension. However, clinical symptomatology is of limited
value in the differentiation of VT from supraventricular
tachycardia (SVT) since similar symptoms may be presented by
patients with either of these conditions.
In order to accurately treat and
manage patient with wide-complex tachycardia, it is critical
that the underlying rhythm is accurately diagnosed, especially
when the patient is hemodynamically unstable. A wide-complex
tachycardia should be presumed to be a VT until the presence
of SVT can be proven, because medications routinely used to
treat SVT can cause severe hemodynamic deterioration by
inducing a relatively stable rhythm of VT to degenerate into
ventricular fibrillation. Patients with a wide-complex
tachycardia in an unstable condition should receive immediate
electrical cardioversion. In accordance with the ACLS
guidelines[1], amiodarone, procainamide, or lidocaine may be
used in patients with a stable VT or a wide-complex
tachycardia of unclear origin.
To date, several studies have
attempted to improve the diagnostic accuracy of
differentiating VT from SVT in the evaluation of wide-complex
tachycardia. Of these, Brugada proposed one of the most
well-recognized 4 characteristics [2]:
- If an RS complex cannot be
identified in any precordial lead, VT can be diagnosed with
a specificity of 100% and a sensitivity of 21%.
- If an RS complex is clearly
distinguished in one or more precordial leads, the interval
between the onset of the R wave and the deepest part of the
S wave (RS interval) is measured. If the RS interval is
greater than 100 milliseconds, VT can be diagnosed with a
specificity of 98% and a sensitivity of 66%.
- If the RS interval is less than 100
milliseconds, the presence or absence of atrioventricular
(AV) dissociation must be determined. Evidence of AV
dissociation is 100% specific and 82% sensitive for VT. This
is because AV dissociation does not occur in SVT.
- If the RS interval is less than 100 milliseconds, and if
AV dissociation cannot be clearly demonstrated, the QRS
morphology may be evaluated. Morphologic criteria suggestive
of VT are extensive and complex, and they should be
evaluated in conjunction with a cardiologist, if necessary.
Other characteristic ECG findings that may assist in the
quick differentiation of VT from SVT include the
following[3,4]:
• An extreme rightward axis (-90 to -180 degrees) is often
more suggestive of VT.
- A slight irregularity of the RR
intervals, especially in the early stages before settling
into a regular rhythm, can be suggestive of VT.
- The width of the QRS complex can
also be useful for distinguishing SVT from VT. In general, a
wide QRS complex greater than 140 milliseconds suggests VT;
however, a QRS duration of less than 140 milliseconds is not
helpful for excluding ventricular tachycardia, because VT is
sometimes associated with a relatively narrow QRS complex.
- If the degree of voltage change in
the first 40 milliseconds of the QRS complex is less than
the degree of voltage change in the last 40 milliseconds of
the complex, this finding is suggestive of VT.
- "Fusion" occurs when a
supraventricular impulse reaches the AV node simultaneously
with a ventricular impulse. Intermittent fusion beats during
a wide-complex tachycardia indicate atrioventricular
dissociation and, therefore, also indicate VT.
- A "capture beat" occurs when a supraventricular rhythm
briefly conducts in a normal fashion, with a resultant
normal QRS complex. The term "capture beat" implies that the
normal conduction system has momentarily replaced the
control of a ventricular focus; hence, VT is present.
In addition, more recently, a study found that VT mechanism
was predicted by the
following[5]:
- Presence of an initial R wave in
aVR
- Width of an initial r or q wave
>40 ms in aVR
- Notching on the initial downstroke of a predominantly
negative QRS complex in aVR
In conclusion, this patient with ventricular tachycardia;
as diagnosed through a ventricular rate of greater than 100
bpm and wide QRS morphology with no regular P waves, as
indicated with a 12-leads ECG; presented with an episode of
severe lightheadedness, unconscious and low blood pressure. An
electrophysiological study was performed, and an
arrhythmogenic focus identified. As a result the patient had
an automatic internal cardiac defibrillator placed and was
followed up as an outpatient.
< References
>
- Wellens HJ. Electrophysiology:
Ventricular tachycardia: diagnosis of broad QRS complex
tachycardia. Heart. 2001;86:579-585.
- Brugada P, Brugada J, Mont L,
Smeets J, Andries EW. A new approach to the differential
diagnosis of a regular tachycardia with a wide QRS complex.
Circulation. 1991;83:1649-1659.
- Akhtar M, Shenasa M, Jazayeri M,
Caceres J, Tchou PJ. Wide QRS complex tachycardia.
Reappraisal of a common clinical problem. Ann Intern Med.
1988;109:905-912.
- Gupta AK, Thakur RK. Wide QRS
complex tachycardias. Med Clin North Am. 2001;85:245-66.
- Vereckei A, Duray G, Szenasi G, et al. New algorithm
using only lead aVR for differential diagnosis of wide QRS
complex tachycardia. Heart Rhythm. Jan
2008;5(1):89-98.
|