Download Week 6 File - ACI Moodle

EMERGENCY MEDICINE
Liverpool Hospital
The Weekly Probe
4th March 2014
Volume 17 Issue 6
Critical Care Access Team (CCAT) – there is a new team of medical and nursing staff , which
although originating from the ICU, aims to improve the flow of critical care patients around Liverpool
Hospital- initially 1000 – 2230 hours 7 days per week. Their priorities are:
1. Medical Emergency Team (MET) response
2. Retrieval of ICU patient from Emergency Department
3. FastTrack bed staffing (pending review of ICU Fast Track policy)
4. Support for ED during peak resuscitation demand - when two (2) or more patients requiring
intensive care level management are present in the ED..
5. Support patient discharge and transfer from ICU post medical clearance
6. ICU clinical support education and patient care assistance
In the event of competing demands on the CCAT that include a patient in ED, discussion must take
place between senior ED and ICU medical staff to ensure ongoing care of the patient(s). So this is a
service you can access when overwhelmed by a number of critically unwell patients.
Orthopaedic referrals _ When referring people to an orthopaedic surgeon for out-patient follow up,
can you please refer to the consultant on-call that day (unless they already have a relationship with
a different surgeon).
Also, please ensure that they have a copy of their images provided on CD – our radiology department
can facilitate this.
Triple I – community Nursing Referrals - For ED patients that we want to send home for
community dressings, IV antibiotics etc (eg for patients out of area and ambulatory care cannot look
after),
We need to fill in the triple I form.
You can get the form via the Liverpool Ed intranet site (Administrative – Discahrge and Ambulatory
care) or on intranet/forms/triple I (SSWAHS).
 Most importantly we need to fill in the ambulatory care treatment/medication authority sheet.
 Fax papers to the number written on the Triple I form.
 Original form to patient.
 Copies to patient files.
 Medication for patient to take home if required. (eg IV antibiotics for nurse to administer)
THIS WEEK
Last weeks case – Brugada syndrome
Next Week’s case
Joke / Quote of the Week
The Week Ahead
LAST WEEK’S CASE – Brugada Syndrome
24yo Anglo-Saxon man presents “post-ictal” after 5 minute seizure / apnoeic episode. He has been
given midazolam 5mg by the ambos - GCS 13 BP 105
This is a copy of his ECG
We often see patients who present with syncope or palpitations. They should all have a ECG
performed and after reviewing this systematically, we should look for a number of abnormalities
including PR interval, long QT interval, WPW. Another abnormality we should look for are changes
suggestive of Brugada syndrome - one of the causes of dysrhythmic sudden cardiac death in young
adults with structurally normal hearts that has only been described recently – first by Pedro and Josep
Brugada in 1992.
So what ? The mortality rate for untreated Brugada syndrome may be as high as 10% per year, even
in asymptomatic patients with typical findings on the resting ECG. Brugada syndrome may be
responsible for 4%-12% of all sudden cardiac deaths and up to 20% of SCD in individuals with
structurally normal hearts. Long QT syndrome, dysrhythmogenic right ventricular cardiomyopathy,
pre-excitation syndromes and idiopathic ventricular fibrillation make up the rest.
Who? Epidemiology and inheritance
Brugada syndrome is most prevalent in young adult males of Southeast Asian descent, but it has
been documented in both genders (males 8 times as common), all age groups (average age 40yo)
and a variety of ethnic populations. It follows an autosomal dominant inheritance pattern with
variable penetrance and expression. The remaining 50% of cases have no family history. As a
result of this SE Asian distribution there are a couple of names given to this sudden cardiac death Philippines -bangungut (“to rise and moan in sleep”), in Japan - pokkuri (not potpurri) (“sudden and
unexpectedly ceased phenomena”), Thailand - Lai Tai (“death during sleep”) as compared with Mai
tai (which means to feel as though you’re dead after drinking too many cocktails)
Why ? Pathophysiology
It appears that sodium channels of the right ventricular epicardium are affected and those in the
endocardium are not. This alteration of action potential in the epicardium but not in the endocardium
causes differential repolarization and refractoriness across the myocardium, leading to a vulnerable
period during which a premature impulse or extra-systole can trigger a re-entrant dysrhythmia.
Sodium-channel dysfunction may be intermittent and consequently so can the ECG abnormalities,
resulting in concealed forms of Brugada syndrome.
Certain physiological and external factors can unmask or exacerbate the channel dysfunction. Many
clinical situations may unmask or exacerbate the ECG pattern of Brugada syndrome. Examples are
Editor: Peter Wyllie
use of sodium-channel blockers, a febrile state, use of vagotonic agents, use of alpha-adrenergic
agonists, use of beta-adrenergic blockers, use of tricyclic antidepressants, use of a combination of
glucose and insulin, hyperkalaemia, hypokalaemia, hypercalcaemia,calcium channel blockers, local
anesthetics (bupivacaine), opioid analgesics (propoxyphene), propofol, potassium channel activators
(pinacidil), antihistamines lithium,and alcohol or cocaine intoxication electrocardiogram is variable
over time, depending on the autonomic interaction and the administration of antiarrhythmic drugs
In this case, the patient was taking both fluoxetine (selective serotonin reuptake inhibitor) and
nortriptyline (TCA) .
Note that the majority of congenital Brugada syndrome patients are believed to possess a structurally
normal heart, consistent with the notion that this is a primary electrical heart disease
Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it (There
is a case report of a patient who died while shaving, presumed due to the vagal stimulation of the
carotid sinus massage). The administration of class Ia, Ic and III drugs increases the ST segment
elevation, and also fever. Exercise decreases ST segment elevation in some patients but increases it
in others (after exercise when the body temperature has risen). The changes in heart rate induced by
atrial pacing are accompanied by changes in the degree of ST segment elevation. When the heart
rate decreases, the ST segment elevation increases and when the heart rate increases the ST
segment elevation decreases. However, the contrary can also be observed. There also appears to
be a circadian pattern with more events occurring during sleep or rest when there is less sympathetic
activity.
ECG - The ECG manifestations of the Brugada syndrome when concealed can be unmasked by
sodium channel blockers, a febrile state, or vagotonic agents. Three types of repolarization patterns
in the right precordial leads (V1-3) are recognized.
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Type 1 ST-segment elevation is diagnostic of Brugada syndrome and is characterized by a
coved (convex upwards) ST-segment elevation >=2 mm (0.2 mV) (downsloping) followed by
a negative T wave. The ST changes are different from the ones observed in acute septal
ischemia, pericarditis, ventricular aneurysm and in some normal variants like early
repolarization. The prominent S wave in the lateral precordial leads (typical of RBBB) is often
absent in Brugada , suggesting this may not be true RBBB.
Type 2 ST-segment elevation has a saddleback appearance with a high take-off ST-segment
elevation of >=2 mm followed by a trough displaying >=1 mm ST elevation followed by either
a positive or biphasic T wave.
Type 3 ST-segment elevation has either a saddleback or coved appearance with an STsegment elevation of <1 mm.
These three patterns may be observed sequentially in the same patient or following the introduction
of specific drugs- thus the ECG can change. Note that Type 2 and 3 ST-segment elevation should not
be considered diagnostic of the Brugada syndrome - a Brugada ECG refers to the manifestation of a
Type 1 ST-segment elevation.
Brugada syndrome is definitively diagnosed when a Type 1 ST-segment elevation (Brugada ECG) is
observed in more than one right precordial lead (V1-V3), in the presence or absence of sodium
channel blocking agent, and in conjunction with one or more of the following: documented VF,
polymorphic ventricular tachycardia (VT); a family history of SCD (<45 years old); coved-type ECGs
in family members; inducibility of VT with programmed electrical stimulation (PES); syncope; or
nocturnal agonal respiration. Drug-induced conversion of Type 3 to Type 2 ST-segment elevation is
considered inconclusive for diagnosis of Brugada syndrome.
Editor: Peter Wyllie
Interesting to note that subsequent ECGs on the same patient showed three different patterns. The
first one on the 12 lead ECG shown above on presentation with the type 1 changes, and the next 2
over the following 2 days
Editor: Peter Wyllie
Provocative pharmacological test involve intravenous flecainide 2 mg/kg over 10 min, maximum 150
mg or procainamide 10mg/kg over 10 min- yet it is important to recognize that the sensitivity of these
criteria in the identification of affected individuals is still undefined and it is certainly lower than 100%One study suggested that the response to a provocative test has a sensitivity of 77% in the subgroup
of patients carrying a mutation in the SCN5A gene
Placement of the right precordial leads in a superior position (up to the 2 nd intercostal spaces above
normal) can increase the sensitivity of the ECG for detecting the Brugada phenotype in some
patients, both in the presence or absence of a drug challenge. Studies are underway to ascertain
whether the greater sensitivity is at the cost of a lower specificity and whether a Type I ECG in the
elevated leads is as predictive of events as a Type I ECG in standard leads.
Is the 1st ECG RBBB? According to Dr Smith’s ECG blog “a non-pathologic RBBB has an rSR’ in V1V3 and no ST elevation anywhere on the ECG. In RBBB, an absence of an r-wave in lead V1 only
may be normal, but if it extends to V2 and beyond it is always abnormal, and the differential includes
not only RBBB with MI but also RBBB with left ventricular hypertrophy, and RBBB with
cardiomyopathy. There is usually up to 1 mm of ST depression in V2 and V3, discordant (opposite
direction of) the positive R’ wave. If there is a very large voltage R’ wave, as in right ventricular
hypertrophy, this ST depression may be greater than 1mm in the absence of acute ischemia. To
determine the presence or absence of ST elevation in RBBB, one must first determine the end of the
QRS, which is the beginning of the ST segment (the J-point)”.
Remember that the ECG in patients with Brugada Syndrome can change over time . It can
be normal at times, and is dynamic, inducible by certain drugs or physiologic conditions.
Clinical presentation - Potentially lethal cardiac dysrhythmias, notably polymorphic ventricular
tachycardia, may occur. If such dysrhythmias terminate spontaneously, patients may present with
palpitations or syncope; if these dysrhythmias persist, they eventually degenerate into VF. A
polymorphic VT resembling a rapid Torsade de Pointes arrhythmia is most commonly associated with
the Brugada syndrome. Monomorphic VT is observed infrequently and is generally more prevalent in
children and infants. VT/VF often terminates spontaneously in patients with the Brugada syndrome.
This may explain why patients wake up at night after episodes of agonal respiration caused by the
arrhythmia. Reports also indicate ~ 20% of Brugada syndrome patients also develop supraventricular
arrhythmias.
Look for other causes of right precordial lead ST-segment elevations .
Editor: Peter Wyllie
Drug Induced Brugada like Syn
 Antiarrhythmics – Na blockers / class 1c drugs (flecanide) / 1A drugs (procainamide) / Ca
channel blockers / B-blockers
 Anti-anginals – nitrates / nicorandil
 Psychotropics – TCAs / SSRIs / Lithium / phenothiazines
 Others – H1 antagonists / cocaine
Treatment
To date, no pharmacological agents have improved survival, however implantable cardiac
defibrillators reduce 10-year mortality to ~ 0%
(1) Symptomatic patients displaying the Type 1 ST-segment elevation or Brugada ECG (either
spontaneously or after sodium channel blockade) who present with aborted sudden death should
receive an ICD as a Class I indication without additional need for EPS. Similar patients presenting
with related symptoms such as syncope, seizure, or nocturnal agonal respiration should also
undergo ICD implantation as a Class I indication after non-cardiac causes of these symptoms have
been carefully ruled out. EPS is recommended in symptomatic patients only for the assessment of
supraventricular arrhythmia.
(2) Asymptomatic patients displaying a Brugada ECG (spontaneously or after sodium channel
block) should undergo EPS if there is a family history of sudden cardiac death suspected to be due
to Brugada syndrome. EPS may be justified when the family history is negative for sudden cardiac
death if the Type 1 ST-segment elevation occurs spontaneously. If inducible for ventricular
arrhythmia, the patient should receive an ICD. This was recommended as a Class IIa indication for
patients presenting with a spontaneous Type I ST-segment elevation and as a Class IIb for patients
who display a Type I ST-segment elevation only after sodium block challenge. More recent data
have called these recommendations into question and suggest that it might be more appropriate to
consider both as Class IIb indications.
Agents that increase the calcium current, such as [beta]-adrenergic agents like isoproterenol, are
useful as well. Isoproterenol, sometimes in combination with quinidine, has been shown to be
effective in normalizing ST-segment elevation in patients with the Brugada syndrome and in
controlling electrical storms, particularly in children
Refs:
Editor: Peter Wyllie
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The Brugada syndrome. [Review] Current Opinion in Cardiology. 22(3):163-70, 2007 May.
Canadian Journal of Emergency Medicine Sept 05 by Watrich, Wood and Steiner
Antzelevitch C. Brugada syndrome. Pacing & Clinical Electrophysiology.
Drug Induced Brugada Syndrome, Yap et al, Europace 2009, 989-994
NEXT WEEK’S CASE
You may have seen this one before but it was a new one for me. A community nurse sends a patient
in for removal of a drain inserted for a bile leak. They have tried albeit unsuccessfully. It is not stitched
in. Other than pulling extremely hard , how do you remove his drain?
JOKE / QUOTE OF THE WEEK
Please forward any funny and litigious quotes you may hear on the floor (happy to publish names if
you want)
THE WEEK AHEAD
Tuesdays - 12:00 – 13:45 Intern teaching -Thomas & Rachel Moore
Wednesday
0800-0900 Critical Care Journal Club. ICU Conf Room / 12.00-1.15 Resident MO in
Thomas & Rachel Moore
Thursday 0730-0800 Trauma Audit. Education Centre / 0800-0830 MET Review Education centre /
1300-1400 Medical Grand Rounds. Auditorium.
Editor: Peter Wyllie