Dan Pixley 2018
 common; about 3–5% of ED visits and 1–6% of
hospital admission
 underlying cause: unknown (34-36%),
vasovagal (18-21%), and cardiac (9.5-18%)
 4 Diagnostic categories:
◦ Reflex-mediated
◦ Orthostatic
◦ Cardiac
◦ Cerebrovascular
 is a rule for evaluating the risk of adverse
outcomes in patients presenting with syncope
 CHESS
◦ Congestive heart failure
◦ Hematocrit < 30%
◦ Abnormal ECG
◦ Shortness of breath
◦ Triage systolic blood pressure < 90
 96% sensitive and 62% specific
 99.2% negative PV, 24.8% PPV
 Can Quick BRAD Walk Home
◦ Conduction blocks
◦ Long/ short QT
◦ Brugada
◦ RV infarction/ coronary ischaemia
◦ ARVD
◦ DCM
◦ WPW
◦ Hypertrophy (HCM or LVH due to AS)
 Age
 History of arrhythmias, IHD, structural Heart disease
 Diabetes
 newly abnormal ECG
 Elevated troponin level
 History of Cardiac disease
 Patients with pacemakers or other cardiac devices:
◦ have a high index of suspicion in these patients for
arrhythmia and / or cardiac device malfunction
◦ All patients with pacemakers with unexplained collapse
must be admitted until such time as their pacemaker can be
checked
◦ Most devices can be interrogated for a record of significant
arrhythmia over an extended period of weeks
 65 year old male with history of
hypercholesterolaemia, HTN and T2DM
presents with epigastric pain.
What do we do?
 74 year old male with history of COPD, HTN
and IHD presents with sharp/central chest
pain of 30 mins duration and then a short
syncope. HR 72, BP 105/62,sats 95% RA
What do we do?
Image from ref 2
 40-50% of all myocardial infarctions
 Up to 40% of patients with an inferior STEMI will
have a concomitant right ventricular infarction
◦ can develop severe hypotension in response to nitrates and generally have
◦ develop significant bradycardia due to second-or third-degree AV block
 RV infarction suggested by
- ST elevation in lead III > lead II
- Presence of reciprocal ST depression in lead I
- Signs of right ventricular infarction: STE in V1 and V4R
 48 year old female with a history of IHD
presents with left sided chest pain radiating
to jaw. Not relieved by normal GTN
What do we do?
Image from ref 1
 Widespread horizontal ST depression, most
prominent in leads I, II and V4-6
 ST elevation in aVR ≥ 1mm
Requires Urgent referral to Cardiology for PCI
 65 year old male with history of T2DM and
smoking self presents after an episode of
chest pain + syncope. The chest pain
resolved 30 mins prior to arrival in ED
 pattern of deeply inverted or biphasic T waves in
V2-3,
 specific for a critical stenosis of the left anterior
descending artery (LAD)
 Patient may be pain free by the time ECG is taken
but they are at extremely high risk for extensive
anterior wall MI within the next few days to
weeks.
 Require PCI
 35 year old male with nil medical history
presents after his bucks party with
palpitations.
 most common sustained arrhythmia
 Lifetime risk over the age of 40 years is ~25%
 Ischaemic heart disease
 Hypertension
 Valvular heart disease (esp. mitral stenosis / regurgitation)
 Acute infections
 Electrolyte disturbance (hypokalaemia, hypomagnesaemia)
 Thyrotoxicosis
 Drugs (e.g. sympathomimetics)
 Pulmonary embolus
 Pericardial disease
 Acid-base disturbance
 Pre-excitation syndromes
 Cardiomyopathies: dilated, hypertrophic.
 Phaeochromocytoma
Reference 2
 47 year old accountant presents SOB pus
presyncopal
 The atria contract at 300 beats per minute
causing a ‘seesaw’ baseline. Beats are
transmitted with a 2:1, 3:1 or 4:1 block,
leading to ventricular rates of 150, 100 and
75 BPM respectively.
 Vagal manouvers +/- Adenosine. A flutter
will not usually respond to this. This will
often give a transient period of increased AV
block during which flutter waves may be
unmasked.
Reference 2
 82 year old male with COPD presents with
fevers and green sputum.
 occurs in respiratory disease and reflects an aberrant foci
of atrial excitation
 typically a transitional rhythm between frequent premature
atrial complexes (PACs) and atrial flutter / fibrillation
 At least 3 distinct P-wave morphologies in the same lead
 Thought to be a result of:
◦ Right atrial dilatation (from cor pulmonale)
◦ Increased sympathetic drive
◦ Hypoxia and hypercarbia
◦ Beta-agonists
Reference 2
 65 year old man with a history of ischaemic
heart disease is found unresponsive.
What do we do?
 65 year old man with a history of ischaemic
heart disease presents with SOB
What do we do?
 Treatment of FBI:
Unstable
◦ DC Cardioversion!
 Stable
◦ IV chemical cardioversion e.g procainamide
◦ Avoid all AV nodal blockers!
 Adenosine
 Verapamil
 Diltiazem
 Beta-blockers
 Digoxin
 Amiodarone (has both beta-blocker and Ca-channel blocker
properties)
 50 year old lady comes to the emergency department from
her husband’s funeral with a sensation of ‘fluttering’ in her
chest. She is feeling very anxious.
What do we do?
2 main types. AVNRT (left) and AVRT (right)
Reference 2
 60 year old male presents with chest pain and
suddenly stops talking during ECG
What do we do?
 18 year old male signs up for the army and
has a routine ECG
 Due to a mutation in the cardiac sodium channel
gene
 Type 1 Coved ST segment elevation >2mm in >1
of V1-V3 followed by a negative T wave
 Type 2: 2mm of saddleback shaped ST elevation
 Diagnosis must be coupled with clinical criteria:
VF, FHX sudden death, Syncope
 The only proven therapy is an implantable
cardioverter – defibrillator (ICD)
 24 year old male collapses 1 minute in to his
run. Has happened previously
 Number one cause of sudden cardiac death in
young athletes. Annual mortality is estimated at
1-2 %
 Left ventricular hypertrophy (LVH), occurring in
the absence of any inciting stimulus such as
hypertension or aortic stenosis
 ECG Signs:
◦ LVH
◦ deep, narrow (“dagger-like”) Q waves in the lateral (V5-
6, I, aVL) and inferior (II, III, aVF) leads
◦ P mitrale
◦ T wave inversion laterally in apical HCM
 A 25 year old man presents with a collapse which
occurred as he was playing in a football match. He
has suffered episodes of fainting in the past
 PR interval <120ms
 Delta wave – slurring slow rise of initial
portion of the QRS
 QRS prolongation >110ms
 Look for T waves in anterior leads. Pre-
excitations simulates RVH
16 year old boy presents to clinic
after an episode of syncope
 Calculate the QTc
◦ Bazetts formula (med calc)
◦ Fredericas formula
 The QT shortens at faster heart rates
 The QT lengthens at slower heart rates
 Bazetts formula not as accurate outside HR 60-100BPM
 QTc is prolonged if > 440ms in men or > 460ms in
women
 QTc > 500 is associated with increased risk of torsades de
pointes
 A useful rule of thumb is that a normal QT is less than half
the preceding RR interval
 Causes:
 Hypokalaemia
 Hypomagnesaemia
 Hypocalcaemia
 Hypothermia
 Myocardial ischemia
 Post-cardiac arrest
 Raised intracranial pressure
 Congenital long QT syndrome
 DRUGS
 K+ channelopathy
 QTc (<300-350)
 Short QT interval
 Lack of the normal changes in QT interval
with heart rate
 Peaked T waves, particularly in the precordial
leads
 Short or absent ST segments
 Episodes of atrial or ventricular fibrillation
20 year old male presents with palpitations
 inherited disorder associated
with paroxysmal ventricular
arrhythmias and sudden cardiac death.
 Epsilon wave (most specific finding, seen in
30% of patients)
 T wave inversions in V1-3 (85% of patients)
 Slurred S wave (V1-3): 95% of patients
 Localised QRS widening of 110ms in V1-3
 Paroxysmal episodes of ventricular
tachycardia
 1st degree:
 2nd degree
◦ Mobitz 1
Mobitz 2
3rd Degree
 60 year old male presents to ED after
syncope. History of CKD.
 Increased extracellular potassium reduces
myocardial excitability.
 leads to suppression of impulse generation
by the SA node and reduced conduction
system, resulting in bradycardia, conduction
blocks and ultimately cardiac arrest.
 Serum potassium > 5.5 mEq/L is associated with repolarization
abnormalities:
◦ Peaked T waves
 Serum potassium > 6.5 mEq/L is associated with progressive
paralysis of the atria:
◦ Lengthen PR, P wave widens and flattens
 Serum potassium > 7.0 mEq/L is associated with conduction
abnormalities and bradycardia:
◦ Prolonged QRS interval with bizarre QRS morphology
◦ High-grade AV block with slow junctional and ventricular escape rhythms
◦ Sinus bradycardia or slow AF
◦ Development of a sine wave appearance (a pre-terminal rhythm)
 Serum potassium level of > 9.0 mEq/L causes cardiac arrest due
to:
 Asystole
 Ventricular fibrillation
 PEA with bizarre, wide complex rhythm
 26 year old male with Conns syndrome
presents with muscle weakness and pains
Hypokalaemia
 A 29 year old BIBA in arrest. Initial ECG done
prior to arrest was this
 ECG done 2 weeks ago by GP was found. She
had presented with chest pain.
 An 18 year old lady is found collapsed at
home. When you see her she has a GCS of 10
and you notice that her pupils are dilated.
 A,B,C,D,E (ventilation may be required)
◦ Bloods including paracetamol level; Activated
charcoal if within 8hrs of ingestion
 Sodium bicarbonate (50ml of 8.4%)
◦ Give if any arrhythmia or QRS widening
 Further options:
◦ If seizures: benzodiazepines
55 year old male with hx of PCKD presents with GCS 3
 82 year old male presents with syncope
84 year old male with hx of CCF plus IHD presents post syncope
 Important ECG findings in Syncope:
◦ Paroxysmal or sustained dysrhythmia on monitoring in clinic
◦ Non-sinus rhythm of any sort
◦ Nonspecific intraventricular conduction delay (QRS > 100 ms without left
or right bundle branch pattern)
◦ Left bundle branch block or left anterior or posterior hemiblock
◦ ECG signs of coronary ischemia
◦ Long QT syndrome - QTc > 440-450 msec in men or > 460 msec in
women
◦ Brugada sign - right bundle branch block and anterior ST elevation
◦ Left ventricular hypertrophy in someone with no reason to have it and/or
Q waves in II, III, aVF, V5, and V6
◦ Pre-excitation syndromes (PR interval < 120 msec) with or without delta
wave
◦ Can Quick BRAD Walk Home
 1. OME – Oxford Medical Education: ECGs and
knowledge
 2. Life in the fast lane – ECG diagnoses A-Z
 3. Prospective validation of the San Francisco
Syncope Rule to predict patients with serious
outcomes. AAEM 2013.
Image from ref 1

Syncope and the ECG

  • 1.
  • 4.
     common; about3–5% of ED visits and 1–6% of hospital admission  underlying cause: unknown (34-36%), vasovagal (18-21%), and cardiac (9.5-18%)  4 Diagnostic categories: ◦ Reflex-mediated ◦ Orthostatic ◦ Cardiac ◦ Cerebrovascular
  • 5.
     is arule for evaluating the risk of adverse outcomes in patients presenting with syncope  CHESS ◦ Congestive heart failure ◦ Hematocrit < 30% ◦ Abnormal ECG ◦ Shortness of breath ◦ Triage systolic blood pressure < 90  96% sensitive and 62% specific  99.2% negative PV, 24.8% PPV
  • 6.
     Can QuickBRAD Walk Home ◦ Conduction blocks ◦ Long/ short QT ◦ Brugada ◦ RV infarction/ coronary ischaemia ◦ ARVD ◦ DCM ◦ WPW ◦ Hypertrophy (HCM or LVH due to AS)
  • 7.
     Age  Historyof arrhythmias, IHD, structural Heart disease  Diabetes  newly abnormal ECG  Elevated troponin level  History of Cardiac disease  Patients with pacemakers or other cardiac devices: ◦ have a high index of suspicion in these patients for arrhythmia and / or cardiac device malfunction ◦ All patients with pacemakers with unexplained collapse must be admitted until such time as their pacemaker can be checked ◦ Most devices can be interrogated for a record of significant arrhythmia over an extended period of weeks
  • 8.
     65 yearold male with history of hypercholesterolaemia, HTN and T2DM presents with epigastric pain. What do we do?
  • 9.
     74 yearold male with history of COPD, HTN and IHD presents with sharp/central chest pain of 30 mins duration and then a short syncope. HR 72, BP 105/62,sats 95% RA What do we do? Image from ref 2
  • 10.
     40-50% ofall myocardial infarctions  Up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction ◦ can develop severe hypotension in response to nitrates and generally have ◦ develop significant bradycardia due to second-or third-degree AV block  RV infarction suggested by - ST elevation in lead III > lead II - Presence of reciprocal ST depression in lead I - Signs of right ventricular infarction: STE in V1 and V4R
  • 11.
     48 yearold female with a history of IHD presents with left sided chest pain radiating to jaw. Not relieved by normal GTN What do we do? Image from ref 1
  • 12.
     Widespread horizontalST depression, most prominent in leads I, II and V4-6  ST elevation in aVR ≥ 1mm Requires Urgent referral to Cardiology for PCI
  • 13.
     65 yearold male with history of T2DM and smoking self presents after an episode of chest pain + syncope. The chest pain resolved 30 mins prior to arrival in ED
  • 14.
     pattern ofdeeply inverted or biphasic T waves in V2-3,  specific for a critical stenosis of the left anterior descending artery (LAD)  Patient may be pain free by the time ECG is taken but they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.  Require PCI
  • 16.
     35 yearold male with nil medical history presents after his bucks party with palpitations.
  • 17.
     most commonsustained arrhythmia  Lifetime risk over the age of 40 years is ~25%  Ischaemic heart disease  Hypertension  Valvular heart disease (esp. mitral stenosis / regurgitation)  Acute infections  Electrolyte disturbance (hypokalaemia, hypomagnesaemia)  Thyrotoxicosis  Drugs (e.g. sympathomimetics)  Pulmonary embolus  Pericardial disease  Acid-base disturbance  Pre-excitation syndromes  Cardiomyopathies: dilated, hypertrophic.  Phaeochromocytoma Reference 2
  • 18.
     47 yearold accountant presents SOB pus presyncopal
  • 19.
     The atriacontract at 300 beats per minute causing a ‘seesaw’ baseline. Beats are transmitted with a 2:1, 3:1 or 4:1 block, leading to ventricular rates of 150, 100 and 75 BPM respectively.  Vagal manouvers +/- Adenosine. A flutter will not usually respond to this. This will often give a transient period of increased AV block during which flutter waves may be unmasked. Reference 2
  • 20.
     82 yearold male with COPD presents with fevers and green sputum.
  • 21.
     occurs inrespiratory disease and reflects an aberrant foci of atrial excitation  typically a transitional rhythm between frequent premature atrial complexes (PACs) and atrial flutter / fibrillation  At least 3 distinct P-wave morphologies in the same lead  Thought to be a result of: ◦ Right atrial dilatation (from cor pulmonale) ◦ Increased sympathetic drive ◦ Hypoxia and hypercarbia ◦ Beta-agonists Reference 2
  • 22.
     65 yearold man with a history of ischaemic heart disease is found unresponsive. What do we do?
  • 23.
     65 yearold man with a history of ischaemic heart disease presents with SOB What do we do?
  • 24.
     Treatment ofFBI: Unstable ◦ DC Cardioversion!  Stable ◦ IV chemical cardioversion e.g procainamide ◦ Avoid all AV nodal blockers!  Adenosine  Verapamil  Diltiazem  Beta-blockers  Digoxin  Amiodarone (has both beta-blocker and Ca-channel blocker properties)
  • 25.
     50 yearold lady comes to the emergency department from her husband’s funeral with a sensation of ‘fluttering’ in her chest. She is feeling very anxious. What do we do?
  • 26.
    2 main types.AVNRT (left) and AVRT (right) Reference 2
  • 27.
     60 yearold male presents with chest pain and suddenly stops talking during ECG What do we do?
  • 28.
     18 yearold male signs up for the army and has a routine ECG
  • 29.
     Due toa mutation in the cardiac sodium channel gene  Type 1 Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave  Type 2: 2mm of saddleback shaped ST elevation  Diagnosis must be coupled with clinical criteria: VF, FHX sudden death, Syncope  The only proven therapy is an implantable cardioverter – defibrillator (ICD)
  • 30.
     24 yearold male collapses 1 minute in to his run. Has happened previously
  • 31.
     Number onecause of sudden cardiac death in young athletes. Annual mortality is estimated at 1-2 %  Left ventricular hypertrophy (LVH), occurring in the absence of any inciting stimulus such as hypertension or aortic stenosis  ECG Signs: ◦ LVH ◦ deep, narrow (“dagger-like”) Q waves in the lateral (V5- 6, I, aVL) and inferior (II, III, aVF) leads ◦ P mitrale ◦ T wave inversion laterally in apical HCM
  • 32.
     A 25year old man presents with a collapse which occurred as he was playing in a football match. He has suffered episodes of fainting in the past
  • 33.
     PR interval<120ms  Delta wave – slurring slow rise of initial portion of the QRS  QRS prolongation >110ms  Look for T waves in anterior leads. Pre- excitations simulates RVH
  • 34.
    16 year oldboy presents to clinic after an episode of syncope
  • 35.
     Calculate theQTc ◦ Bazetts formula (med calc) ◦ Fredericas formula  The QT shortens at faster heart rates  The QT lengthens at slower heart rates  Bazetts formula not as accurate outside HR 60-100BPM  QTc is prolonged if > 440ms in men or > 460ms in women  QTc > 500 is associated with increased risk of torsades de pointes  A useful rule of thumb is that a normal QT is less than half the preceding RR interval
  • 36.
     Causes:  Hypokalaemia Hypomagnesaemia  Hypocalcaemia  Hypothermia  Myocardial ischemia  Post-cardiac arrest  Raised intracranial pressure  Congenital long QT syndrome  DRUGS
  • 38.
     K+ channelopathy QTc (<300-350)  Short QT interval  Lack of the normal changes in QT interval with heart rate  Peaked T waves, particularly in the precordial leads  Short or absent ST segments  Episodes of atrial or ventricular fibrillation
  • 39.
    20 year oldmale presents with palpitations
  • 40.
     inherited disorderassociated with paroxysmal ventricular arrhythmias and sudden cardiac death.  Epsilon wave (most specific finding, seen in 30% of patients)  T wave inversions in V1-3 (85% of patients)  Slurred S wave (V1-3): 95% of patients  Localised QRS widening of 110ms in V1-3  Paroxysmal episodes of ventricular tachycardia
  • 41.
     1st degree: 2nd degree ◦ Mobitz 1 Mobitz 2 3rd Degree
  • 42.
     60 yearold male presents to ED after syncope. History of CKD.
  • 43.
     Increased extracellularpotassium reduces myocardial excitability.  leads to suppression of impulse generation by the SA node and reduced conduction system, resulting in bradycardia, conduction blocks and ultimately cardiac arrest.
  • 44.
     Serum potassium> 5.5 mEq/L is associated with repolarization abnormalities: ◦ Peaked T waves  Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria: ◦ Lengthen PR, P wave widens and flattens  Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia: ◦ Prolonged QRS interval with bizarre QRS morphology ◦ High-grade AV block with slow junctional and ventricular escape rhythms ◦ Sinus bradycardia or slow AF ◦ Development of a sine wave appearance (a pre-terminal rhythm)  Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:  Asystole  Ventricular fibrillation  PEA with bizarre, wide complex rhythm
  • 46.
     26 yearold male with Conns syndrome presents with muscle weakness and pains Hypokalaemia
  • 47.
     A 29year old BIBA in arrest. Initial ECG done prior to arrest was this
  • 48.
     ECG done2 weeks ago by GP was found. She had presented with chest pain.
  • 49.
     An 18year old lady is found collapsed at home. When you see her she has a GCS of 10 and you notice that her pupils are dilated.
  • 50.
     A,B,C,D,E (ventilationmay be required) ◦ Bloods including paracetamol level; Activated charcoal if within 8hrs of ingestion  Sodium bicarbonate (50ml of 8.4%) ◦ Give if any arrhythmia or QRS widening  Further options: ◦ If seizures: benzodiazepines
  • 51.
    55 year oldmale with hx of PCKD presents with GCS 3
  • 52.
     82 yearold male presents with syncope
  • 53.
    84 year oldmale with hx of CCF plus IHD presents post syncope
  • 54.
     Important ECGfindings in Syncope: ◦ Paroxysmal or sustained dysrhythmia on monitoring in clinic ◦ Non-sinus rhythm of any sort ◦ Nonspecific intraventricular conduction delay (QRS > 100 ms without left or right bundle branch pattern) ◦ Left bundle branch block or left anterior or posterior hemiblock ◦ ECG signs of coronary ischemia ◦ Long QT syndrome - QTc > 440-450 msec in men or > 460 msec in women ◦ Brugada sign - right bundle branch block and anterior ST elevation ◦ Left ventricular hypertrophy in someone with no reason to have it and/or Q waves in II, III, aVF, V5, and V6 ◦ Pre-excitation syndromes (PR interval < 120 msec) with or without delta wave ◦ Can Quick BRAD Walk Home
  • 55.
     1. OME– Oxford Medical Education: ECGs and knowledge  2. Life in the fast lane – ECG diagnoses A-Z  3. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. AAEM 2013. Image from ref 1

Editor's Notes

  • #6 99.2% negative PV, 24.8% PPV Which means 24.8% of San Fran rule positive will have serious morbidity or mortality 138/1194 had serious outcome – MI, stroke, death, arrhytmia, PE, SAH or return to ED
  • #10 gxfghxfg
  • #52 Widespread, giant T-wave inversions (“cerebral T waves”) secondary to subarachnoid haemorrhage. The QT interval is also grossly prolonged (600 ms).
  • #53 Massive PE
  • #54 Trifasicular block