4. 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
5. 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
6. 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)
7. 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
8. 65 year old male with history of
hypercholesterolaemia, HTN and T2DM
presents with epigastric pain.
What do we do?
9. 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
10. 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
11. 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
12. 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
13. 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
14. 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
15.
16. 35 year old male with nil medical history
presents after his bucks party with
palpitations.
17. 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
18. 47 year old accountant presents SOB pus
presyncopal
19. 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
20. 82 year old male with COPD presents with
fevers and green sputum.
21. 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
22. 65 year old man with a history of ischaemic
heart disease is found unresponsive.
What do we do?
23. 65 year old man with a history of ischaemic
heart disease presents with SOB
What do we do?
24. 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)
25. 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?
26. 2 main types. AVNRT (left) and AVRT (right)
Reference 2
27. 60 year old male presents with chest pain and
suddenly stops talking during ECG
What do we do?
28. 18 year old male signs up for the army and
has a routine ECG
29. 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)
30. 24 year old male collapses 1 minute in to his
run. Has happened previously
31. 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
32. 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
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 old boy presents to clinic
after an episode of syncope
35. 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
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
40. 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
42. 60 year old male presents to ED after
syncope. History of CKD.
43. 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.
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
45.
46. 26 year old male with Conns syndrome
presents with muscle weakness and pains
Hypokalaemia
47. A 29 year old BIBA in arrest. Initial ECG done
prior to arrest was this
48. ECG done 2 weeks ago by GP was found. She
had presented with chest pain.
49. 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.
50. 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
51. 55 year old male with hx of PCKD presents with GCS 3
53. 84 year old male with hx of CCF plus IHD presents post syncope
54. 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
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
Notas do Editor
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
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Widespread, giant T-wave inversions (“cerebral T waves”) secondary to subarachnoid haemorrhage.
The QT interval is also grossly prolonged (600 ms).