Teaching Clinic - Three Cases with Syncope Flashcards
- Mr. YSM, M/54
- C/O: Sudden onset of palpitation associated with syncope
- Sudden onset of rapid palpitation for 1-2 minutes, associated with mild dyspnea and then LOC
- ? Mild twitching of all 4 limbs during the episode as noted by his wife
- Lasting for 30 seconds and patient spontaneous regain conscious
- No head injury or neurological abnormality after recovery
Hx:
- Head injury-related? Before or after passing out?
- Frequency (with previous recovery = better prognosis, means that patient has survived before vs. first episode may have worse prognosis)
- Previous heart attack
- Exertional angina / dyspnea ?
- Palpitatoins?
- Dizziness?
- LOC? Twitching/tongue-biting/post-ictal drowsiness? Up-rolling eyeballs? Cyanosis?
- Exercise capacity?
- Orthopnea? PND?
- Past history: heart disease? long-term medical therapy?
- Medication causing syncope? (ACEi S/E: first-dose hypotension, hyperkalemia, cough, angioedema, vascular leakage)
- Social history: Smoker? Drinker?
- Family history
- Drug history
- Age (young = vasovagal, inherited conditions [HOCM, Brugada) vs. middle age = structural heart disease)
What does it mean if a patient is twitching but we cannot open their eyes?
This is malingering. Eyes should roll backwards in true syncope.
Eye opening muscles are voluntary muscles.
What happens to blood pressure and breathing pattern during seizure?
- Blood pressure very high (sympathetic tone)
- Patient is not apneic (hypoxemic causing increased sympathetic tone)
Where may cardioembolism lead to syncope?
Brainstem (vertebral circulation) = unusual
When may Afib lead to syncope?
- Slow AF
- Poor ventricular function
- Brainstem stroke
- Sick sinus syndrome (long-pause)
- Wolff-Parkinson-White
How much cardiac output is contributed by atrial contraction?
10%, unless there is problem during filling phase (i.e. HOCM, ventricular dysfunction)
What are fatal conditions which must not be missed in a patient with syncope?
4 conditions that you cannot miss
- Myocardial infarction (1/8 will present with syncope) =60% get to hospital in time, 40% die at home
– Ischaemic-related ventricular fibrillation (can be due to transient ischaemia due to occlusion of arteries) - Pulmonary embolism (1/8 will present with syncope=saddle PE) = haemodynamic collapse. Increased pulmonary arterial pressure causes increased myocardial contraction which breaks up the clot. Syncope is a bad prognostic factor as it indicates a large clot.
- Aortic dissection
- Rhythem problem (slow heart beat or fatal arrhythmia: ventricular arrhythmia, TdP) = ventricular scar [re-entrant related tachycardia = 1-2 years after event]
Relative importance of diagnosis, frequency of disorder, presentation
4 highly fatal conditions that you cannot miss
Rhythm problem (heart block, bradycardia, ventricular rhythm issues), aortic dissection, pulmonary embolism, myocardial inafarction
Patient with MI wakes up. How come?
Spontaneous reperfusion (blood clot resolves) = Regain consciousness (not the entire artery is occluded)
Aortic dissection = Transient dissection (compress on false lumen)
What medication cannot be given with ACEi?
ACEi releases bradykinin
ARNI releases bradykinin (Sacubitril/valsartan)
High risk of angioedema
What 4 drugs are in the heart failure treatment regimen?
ARNI, a beta-blocker, an MRA, and an SGLT2 inhibitor
Drugs that prolong QT
Antibiotics (episodic drug):
- Macrolides
- Quinolones
- Septrin
Anti-psychotics:
Anti-emetic
Anti-depressant
Anti-arrhythmic
- class IA [quinidine]
- class IC [sodium channel blocker, i.e. flecainide]
- class III [i.e. amiodarone],
Drug abuse = methadone, analgesics (prolong QT = sudden death)
Anti-histamine
Anti-spasmodic drugs (GI upset)
TCM (acrolein)
What drug shorten QT?
Class II (B) = propanolol (shorten QT)
class IB [i.e. shorten QT = lidocaine, mexlitine = shorten QT]
Physical examination: conscious and alert
– BP: 110/65, pulse regular 70 bpm, all pulse equal and normal
– Heart sound normal with pansystolic murmur over apex, no carotid bruit
– Chest: mild bilateral basal crepitation
– Neurological examination: NAD
- Pansystolic murmur: malignant MVP syndrome [99% benign,1% malignant] = ventricular premature beat + ventricular arrhythmia
Rate: 85 bpm
Axis: Normal
Rhythm: Regular
Interval: QT 2.2, not prolonged
Chamber enlargement: Left atrial enlargement (mitral regurgitation), no ventricular enlargement
QRS complex: amplitude change & progression, widening of QRS:, L or R bundle, Q wave [V5, V6] = anterolateral , [II, III, aVF] = inferior)
Dx: inferior and anterolateral MI
Rate: 200 bpm
Axis: Extreme axis deviation
Rhyhtm:
Wide complex tachycardia: VT, SVT +/- WPW, BBB, pre-existing wide complex
Anterolateral myocardial infarction
RBBB, so it’s coming from the L-side
RBBB = left VT
7 criteria for VT
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”): QRS positive in aVR and negative in I and aVF
- Very broad complexes > 160ms
- AV dissociation: P and QRS complexes at different rates. P waves are often superimposed on QRS complexes and may be difficult to discern
- Capture beats: Occur when the sinoatrial node transiently “captures” the ventricles in the midst of AV dissociation, producing a QRS complex of normal duration (see 3)
- Fusion beats: Occur when a sinus and ventricular beat coincide to produce a hybrid complex
- Positive or negative concordance throughout the precordial leads, i.e. lead V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen
Rhythm:
Axis: LAD
Fusion beat = VT
Where is VT = RBBB = left VT (septum!) [not lateral]
L-axis (through the spetum)
Value of EP Study in Syncope
Treatment of Previous Myocardial Infarction with Ventricular Tachycardia
- Anti-heart failure
- Anti-ischaemic
- Implantable cardioverter defibrillator
(Give anti-arrhythmic drugs or cath ablation of accessory pathway)
- Axis: RAD
- Chamber enlargement: V1 P wave is very small (monophasic) = R atrial enlargement
- RIght ventricular enlargement:
– Big S wave in V5, V6
– Big S wave in lead I
Q wave in lead III (inverted)
Pulmonary embolism
- Sympathetic activation: sinus tachycardia
- Right ventricular dilatation
Rate:
Rhythm
Axis: RAD
QT: 0.6 (one big square in 0.2, small square is 0.04)
R Atrial Enlargement
R Ventricular Enlargement
S1Q3T3
4 common causes of prolonged QT
- drug
- electrolytes
- ischaemia
- idiopathic
Rate: <60
Axis: LAD
Prolonged PR interval
QRS complex is wide
No monophasic P wave (atrium looks normal)
Left ventricular normal
V2 through V3 (Pathological Q wave)
ST changes: ST elevation in leads V1-6, aVL
Anterolateral STEMI
What could cause exercise-induced syncope?
L-sided obstruction
Atrial myxoma (obstruct L ventricle)
Turner syndrome
R-sided obstructoin
Pulmonary hype
Ventricular arrhythmia, SVT
CPVT
Marfan’s syndrome? Aortic dissection (basketball, super tall)
Think of inherited causes due to father’s abnormal ECG:
- Cardiomyopathy (could be inherited)
- Rhythm problem (long QT, CPVD)
- Pulmonary HT
- Marfan’s syndrome
Rate: 100
Axis: left axis deviation
Rhythm: Irregularly irregular (DDx: AF, MAT, atrial flutter with variable condution)
This is MAT (P wave looks different, look at lead II)
Normal interval
Chamber enlargement: No atrial enlargement, LVH
Pathological Q waves in multiple leads = scarring of muscles (cardiomyopathy)
Bulging of septum = HOCM
What must we think of when there is exercise induced syncope?
Leading causes of SCD in young competitive athletes
How does anomalus origin of coronary artery lead to SCD?
Right come from R side, left come from L side
L-side come from right
Axis: RAD
Rhythm: Irregular
Wide
Irregular wide complex tachycardia:
1. Ventricular arrhythmia
4. AF with something superimposing on AF, i.e. WPW (accessory pathway)
Delta wave +ve in V1 = L-sided WPW
Accessory pathways come from mitral annulus
Pre-excitement AF
V1 P wave is upright = atrial enlargement
RSR’ (big R wave in V1) = RBBB, WPW, RVH, posterior MI
S wave in V1 and V6
Epsilon wave have ARVD (islands on muscles in between fat, small bundle of muscle activating will give rise to small QRS complex = epsilon wave)
We only see epsilon wave in young patients, before the island of muscle dies
Prolonged QT >450 (600)
Drugs
Electrolytes (hypoK)
Long QT = low potassium
Flattened T waves (low potassium)
Low calcium flat T waves
No ST segment changes
No ischaemia
By exclusion, it is either drugs or idiopathic long QT
Rate: 65
Rhythm: sinus rhythm
Axis: RAD
Interval:
- PR prolonged
- QRS prolonged (wide)
- QT normal
Big R-wave in V1
DDx:
- RVH (no big S wave in V1 and V5)
- RBBB (rsr)
- Posterior MI (no ST elevation)
- WPW (must have short PR)
- QRS morphology: wide
- No ST segment changes
First degree heart block, RBBB, RAD = Bifascicular block (1 in 8 will progress into complete heart block)
Most cases, we don’t need to do anything. Need to R/O myocardial ischaemia, must monitor as may become CHB (borderline indication for pacemaker if syncope)
Rate: 50 bpm
Rhythm: p wave not followed by QRS complex (complete heart block, A & V are dissociated)
QRS: normal
QT: QT interval prolongation (with bradycardia, may be slightly prolonged)
Possible feature of electrolyte problem
No Q wave
No ST segment changes
Dx: CHB
Causes of CHB: Electrolyte, MI, drug, degeneration
Rate: Bradycardia
Complete heart block
No PR interval
QRS is wide
When we look for wide QRS (escaped beat from ventricle = unstable, can get to asystole much faster)
Narrow QRS (escaped beat from AV node)
QT is not prolonged
RSR’ = RBBB
Escaped rhythm from L ventricle
Anteroseptal MI has poor prognosis
Inferior STEMI most reversible
Lead III have more ST elevation, R is V3
RCA occlusion (more likely to cause CHB)
Rate:
Rhythm:
Axis:
Chamber enlargement: none
Partial RBBB with RSR’ block (J-point elevation dragged it up)
Type I Brugada Syndrome
Sodium channel blocker
If have J point elevation = hypothermia (but everywhere will have ST segment elevation, there is no localisation)
Rate:
Rhythm: Sinus
Axis: RAD
Interval: Shortened PR, wide QRS,
LVH: big S wave and tall R wave = 7 big squares
Wolff-Parkinson White
- Delta wave is +ve = L-side
- Activating towards R-side
Indication for echocardiography
What is Tilt Table Test for syncope? What are the indications?
How is TTT done?
What are Neurally Mediated Syncopal Syndromes?
- Vasovagal
- Cough
- Exercise-induced
- Glossopharyngeal neuralgia
- Deglutition
- Postprandial
- Micturition
- Carotid sinus
- Orthostatic
Therapy for Neurally-Mediated Syncope
Non-Pharmacological Therapy for Neurally-Mediated Syncope
Non-pharmacological Therapy:
Volume Expansion:
–Increase salt and fluid intake
Tilt Training
Isometric leg and arm counterpressure manoeures
Bradycardia:
–Permanent DDD pacing: frequency, severe attack and age >40
Mannouveres to teach patients to prevent Neurally-Mediated Syncope
Medical therapy for Neurally-Mediated Syncope
Syndromes of orthostatic intolerance that may cause syncope
What are the causes of syncope?
DDx for LOC
Assessment of syncope
Syncope mimics
Syncope vs. Seizures
Value of ECG in evaluating syncope
